Adrenaline-Induced Hypertension in Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 191s-193s ◽  
Author(s):  
L.-H. Tung ◽  
M. J. Rand ◽  
H. Majewski
Keyword(s):  
Blood Pressure ◽  
Feedback Loop ◽  
Chronic Treatment ◽  
Nerve Terminals ◽  
Concomitant Treatment ◽  
Metoprolol Tartrate ◽  
Osmotic Minipumps ◽  
Pressor Responses ◽  
Induced Hypertension ◽  
Blood Pressures

1. Rats implanted with osmotic minipumps delivering adrenaline intraperitoneally at the rate of 2.9 nmol/h had significantly higher systolic and diastolic pressures from days 2 to 6 after implantation than sham-operated control rats. 2. Concomitant treatment with metoprolol tartrate (2.5 mg/kg, intraperitoneally, twice daily) prevented the elevation in blood pressure induced by adrenaline from osmotic minipumps. Such metoprolol treatment did not affect the blood pressure of control rats. 3. Noradrenaline administered intraperitoneally from osmotic minipumps at the rate of 2.9 nmol/h had no significant effect on blood pressure over a 6-day period of observation. 4. Tachyphylaxis developed to the acute pressor responses to intermittent intravenous infusions of adrenaline in doses of 0.78 μg (4.24 nmol) every 10 min, but after 14 days of such treatment systolic and diastolic blood pressures were significantly greater than in control rats. 5. It is suggested that the increase in blood pressure produced by chronic treatment with adrenaline is due to the uptake and accumulation of adrenaline in noradrenergic nerve terminals, from which it is subsequently released as a cotransmitter that mediates a positive feedback loop on, transmission by acting on prejunctional β-adrenoceptors.

A role for thyroid hormones in cold-induced elevation of blood pressure and cardiac hypertrophy

1994 ◽  
Vol 72 (9) ◽  
pp. 1066-1074 ◽  
Author(s):  
Melvin J. Fregly ◽  
Fabian Rossi ◽  
J. Robert Cade
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Thyroid Hormones ◽  
Antithyroid Drug ◽  
Thyroid Stimulating Hormone ◽  
Control Group ◽  
Acute Administration ◽  
Induced Hypertension ◽  
Blood Pressures ◽  
Stimulating Hormone

The systolic blood pressures of two groups of rats that were exposed to cold (5 °C) for 4 weeks were elevated significantly above that of warm-acclimated controls maintained at 24 °C. At this time these groups were given the antithyroid drug aminotriazole in their food at 0.3 g/kg. At the same time, one group was given 15.8 μg thyroxine (T4)/kg body mass per day, while the second received 31.6. The doses were chosen as replacement (15.8 μg/kg) and twice replacement (31.8 μg/kg) for the rats. The results of the study revealed that both groups receiving aminotriazole and T4 had reductions in blood pressure within 1 week of initiation of treatment. Blood pressures reached control level after 5 weeks. Cardiac hypertrophy accompanying cold-induced hypertension was reduced with the lower dose of T4 and prevented with the higher dose. Serum concentrations of T4 and triiodothyronine (T3) in the two treated groups were reduced, while serum thyroid-stimulating hormone concentration and thyroid mass were increased above that of the warm-acclimated control group. This suggests that the rats were hypothyroid relative to the warm-acclimated control group. However, the treated rats grew at the same rate as nontreated, cold-exposed controls and had similar food and water intakes, a similar dipsogenic response to acute administration of isoproterenol, and similar colonic temperatures. These measurements suggest that the rats were not functionally hypothyroid. Nevertheless, the results suggest that a paradigm in which the secretory ability of the thyroid gland is blocked, and T4 is returned at a constant, albeit suboptimal, level, reduced blood pressure and cardiac hypertrophy in cold-exposed rats. Hence, the increased turnover of thyroid hormones that characteristically accompanies exposure to cold plays a role in these changes. These studies also indicate that an increase in the rate of secretion of T4 is not required for survival in cold air.Key words: cold-induced hypertension, thyroxine, triiodothyronine, thyroid-stimulating hormone, aminotriazole, antithyroid drug, blood pressure, cardiac hypertrophy, catecholamines, norepinephrine, epinephrine, dopamine.

scholarly journals INFLUENCE OF DIETARY POTASSIUM AND SODIUM/POTASSIUM MOLAR RATIOS ON THE DEVELOPMENT OF SALT HYPERTENSION

1972 ◽  
Vol 136 (2) ◽  
pp. 318-330 ◽  
Author(s):  
Lewis K. Dahl ◽  
George Leitl ◽  
Martha Heine
Keyword(s):  
Blood Pressure ◽  
Dietary Sodium ◽  
Molar Ratio ◽  
Molar Ratios ◽  
Dietary Potassium ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Blood Pressures ◽  
Absolute Concentrations ◽  
Dietary Sodium Chloride

Among genetically hypertension-prone rats, dietary sodium (chloride) was demonstrably hypertensinogenic and potassium (chloride) antihypertensinogenic. On diets containing the same NaCl but different KCl concentrations, mean blood pressure was greater in rats receiving less dietary potassium, i.e., diets with a higher Na/K molar ratio. On diets with different absolute concentrations of NaCl and KCl, but the same Na/K molar ratios, rats on the higher absolute NaCl intakes had the higher blood pressures. On diets with different absolute concentrations of NaCl and KCl, and different Na/K molar ratios, a group on a lower absolute NaCl intake but with a higher Na/K ratio could have more hypertension than a group on a higher absolute NaCl intake but with a lower Na/K ratio. At equivalent molar ratios, the respective effects of these two ions on blood pressure were dominated by that of sodium. It was concluded that the dietary Na/K molar ratio can be an important determinant for the severity, or even development, of salt-induced hypertension. The mechanism of the moderating effect of potassium on sodium-induced hypertension was unclear.

scholarly journals Differential effects of Mas receptor deficiency on cardiac function and blood pressure in obese male and female mice

2017 ◽  
Vol 312 (3) ◽  
pp. H459-H468 ◽  
Author(s):  
Yu Wang ◽  
Robin Shoemaker ◽  
David Powell ◽  
Wen Su ◽  
Sean Thatcher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Function ◽  
Left Ventricular ◽  
Ang Ii ◽  
Wild Type ◽  
Male And Female ◽  
Reduced Ejection Fraction ◽  
Female Mice ◽  
Induced Hypertension ◽  
Blood Pressures

Angiotensin-(1–7) [ANG-(1–7)] acts at Mas receptors (MasR) to oppose effects of angiotensin II (ANG II). Previous studies demonstrated that protection of female mice from obesity-induced hypertension was associated with increased systemic ANG-(1–7), whereas male obese hypertensive mice exhibited increased systemic ANG II. We hypothesized that MasR deficiency ( MasR−/−) augments obesity-induced hypertension in males and abolishes protection of females. Male and female wild-type ( MasR+/+) and MasR−/− mice were fed a low-fat (LF) or high-fat (HF) diet for 16 wk. MasR deficiency had no effect on obesity. At baseline, male and female MasR−/− mice had reduced ejection fraction (EF) and fractional shortening than MasR+/+ mice. Male, but not female, HF-fed MasR+/+ mice had increased systolic and diastolic (DBP) blood pressures compared with LF-fed controls. In HF-fed females, MasR deficiency increased DBP compared with LF-fed controls. In contrast, male HF-fed MasR−/− mice had lower DBP than MasR+/+ mice. We quantified cardiac function after 1 mo of HF feeding in males of each genotype. HF-fed MasR−/− mice had higher left ventricular (LV) wall thickness than MasR+/+ mice. Moreover, MasR+/+, but not MasR−/−, mice displayed reductions in EF from HF feeding that were reversed by ANG-(1–7) infusion. LV fibrosis was reduced in HF-fed MasR+/+ but not MasR−/− ANG-(1–7)-infused mice. These results demonstrate that MasR deficiency promotes obesity-induced hypertension in females. In males, HF feeding reduced cardiac function, which was restored by ANG-(1–7) in MasR+/+ but not MasR−/− mice. MasR agonists may be effective therapies for obesity-associated cardiovascular conditions. NEW & NOTEWORTHY MasR deficiency abolishes protection of female mice from obesity-induced hypertension. Male MasR-deficient obese mice have reduced blood pressure and declines in cardiac function. ANG-(1–7) infusion restores obesity-induced cardiac dysfunction of wild-type, but not MasR-deficient, male mice. MasR agonists may be cardioprotective in obese males and females.

scholarly journals Role of the Na+/H+ exchanger 3 in angiotensin II-induced hypertension

2015 ◽  
Vol 47 (10) ◽  
pp. 479-487 ◽  
Author(s):  
Xiao C. Li ◽  
Gary E. Shull ◽  
Elisa Miguel-Qin ◽  
Jia L. Zhuo
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Glycogen Synthase ◽  
Proximal Tubules ◽  
Dependent Manner ◽  
Ang Ii ◽  
Lower Systolic Blood Pressure ◽  
Salt Wasting ◽  
Pressor Responses ◽  
Induced Hypertension

The renal mechanisms responsible for angiotensin II (ANG II)-induced hypertension remain incompletely understood. The present study tested the hypothesis that the Na+/H+ exchanger 3 (NHE3) is required for ANG II-induced hypertension in mice. Five groups of wild-type ( Nhe3 +/+) and Nhe3 −/− mice were treated with vehicle or high pressor doses of ANG II (1.5 mg/kg/day ip, via minipump for 2 wk, or 10 pmol/min iv for 30 min). Under basal conditions, Nhe3 −/− mice had significantly lower systolic blood pressure (SBP) and mean intra-arterial pressure (MAP) ( P < 0.01), 24 h urine ( P < 0.05), urinary Na+ ( P < 0.01) and urinary K+ excretion ( P < 0.01). In response to ANG II, SBP and MAP markedly increased in Nhe3 +/+ mice in a time-dependent manner, as expected ( P < 0.01). However, these acute and chronic pressor responses to ANG II were significantly attenuated in Nhe3 −/− mice ( P < 0.01). Losartan blocked ANG II-induced hypertension in Nhe3 +/+ mice but induced marked mortality in Nhe3 −/− mice. The attenuated pressor responses to ANG II in Nhe3 −/− mice were associated with marked compensatory humoral and renal responses to genetic loss of intestinal and renal NHE3. These include elevated basal plasma ANG II and aldosterone and kidney ANG II levels, salt wasting from the intestines, increased renal AQP1, Na+/HCO3−, and Na+/K+-ATPase expression, and increased PKCα, mitogen-activated protein kinases ERK1/2, and glycogen synthase kinase 3αβ signaling proteins in the proximal tubules ( P < 0.01). We concluded that NHE3 in proximal tubules of the kidney, along with NHE3 in intestines, is required for maintaining basal blood pressure as well as the full development of ANG II-induced hypertension.

Abstract P114: Mas Receptor Deficiency Increases Diastolic Blood Pressure and Reduces Cardiac Function in Obese Female Mice

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Yu Wang ◽  
Robin Shoemaker ◽  
Sean Thatcher ◽  
Lisa Cassis
Keyword(s):  
Blood Pressure ◽  
Cardiac Function ◽  
Plasma Concentrations ◽  
Reduce Blood Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Female Mice ◽  
Obese Female ◽  
Induced Hypertension ◽  
Blood Pressures

Objective: We recently demonstrated that protection of female mice from obesity-induced hypertension was associated with increased plasma concentrations of angiotensin-(1-7) (Ang-(1-7)). Ang-(1-7) is a ligand for Mas receptors (MasR), where the peptide has been reported to promote endothelial release of nitric oxide and reduce blood pressure. In this study, we hypothesized that MasR deficiency will abolish protection of female high fat (HF)-fed mice from the development of obesity-induced hypertension. Methods and Results: Female (8 weeks, C57BL/6) wild type (MasR+/+) and whole body MasR deficient mice (MasR-/-) were fed a HF diet (60% Kcal as fat) for 16 weeks. MasR deficiency had no effect on the development of obesity or glucose intolerance in HF-fed female mice. At week 16 of HF feeding, blood pressure was quantified by radiotelemetry. Deficiency of MasR resulted in a significant decrease in pulse pressures of HF-fed females (24hr average: MasR+/+, 37.7 ± 1.5 mmHg; MasR-/-, 33.1 ± 1.0 mmHg; P<0.05). Diastolic blood pressures (DBP) of HF-fed female MasR-/- mice were modestly elevated during the night cycle compared to controls (DBP night: MasR+/+, 91.5 ± 2.0 mmHg; MasR-/-, 96.6 ± 1.3 mmHg; P=0.06). However, systolic blood pressure, mean arterial pressure and heart rate were not significantly different between genotypes. Assessment of left ventricular function by ultrasound demonstrated significant reductions in stroke volume (MasR+/+, 44.3 ± 1.6 μl; MasR-/-, 36.3 ± 2.1 μl), ejection fraction (MasR+/+, 57.1 ± 1.2; MasR-/-, 50.1 ± 2.7%) and fractional shortening (MasR+/+, 29.7 ± 0.8; MasR-/-, 25.3 ± 1.7%) in HF-fed MasR-/- females compared to controls. Conclusion: These results demonstrate that MasR deficiency promotes elevated diastolic blood pressures and reduced cardiac function in obese female mice, suggesting that the Ang-(1-7)/MasR axis protects females from obesity-hypertension. Moreover, these results suggest that MasR agonists may be effective therapies for obesity-associated cardiovascular conditions.

Interaction of hypertension and caloric restriction on cardiac mass and isomyosin expression

1995 ◽  
Vol 268 (1) ◽  
pp. R33-R39 ◽  
Author(s):  
S. J. Swoap ◽  
P. Boddell ◽  
K. M. Baldwin
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Caloric Restriction ◽  
Left Ventricular ◽  
Cardiac Mass ◽  
Aortic Constriction ◽  
Systemic Blood ◽  
Abdominal Aortic ◽  
Induced Hypertension ◽  
Blood Pressures

Previous studies show that elevations in blood pressure induce concomitant increases in both cardiac mass and slow beta-myosin heavy chain (MHC) expression in rodents, whereas caloric restriction of 50% (CR) causes an increase in beta-MHC while modestly lowering blood pressure in normotensive rats. The goals of this study were to 1) determine if beta-MHC expression could be independently regulated by CR and hypertension when these two interventions are combined and 2) determine if CR exerts a lowering of blood pressure in two contrasting models of rodent hypertension. Rodents were assigned to the following groups: 1) normal control (NC); 2) abdominal aortic constriction (Abcon), a model that induces hypertension via renin-angiotensin II; 3) nephrectomy-deoxycorticosterone acetate treatment (DOCA), a model that induces hypertension through increased salt retention; 4) CR; 5) Abcon+CR; 6) DOCA+CR. Results show that both Abcon and DOCA induced significant increases in systemic blood pressures, left ventricular (LV) weight/body weight, and the relative content of beta-MHC compared with NC. When applied in combination with either Abcon or DOCA, CR significantly blunted the changes observed in both systemic blood pressures and LV weight/body weight. In contrast, CR in conjunction with DOCA augmented % beta-MHC expression relative to either DOCA or CR alone. These data suggest 1) caloric restriction exerts a powerful impact on reducing experimentally induced hypertension in rodents and 2) the regulation of beta-MHC expression appears to be regulated by at least two processes, one associated with the stimulus of hypertension and the other involving an independent pathway linked to caloric restriction.

Effect of central infusion of benzamil on Dahl S rat hypertension

1995 ◽  
Vol 269 (3) ◽  
pp. H1044-H1047 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Weight Gain ◽  
Na Channel ◽  
Subcutaneous Infusion ◽  
Intracerebroventricular Infusion ◽  
Significant Difference ◽  
Induced Hypertension ◽  
Blood Pressures

The effect of continuous central infusion of benzamil, a Na+ channel-selective amiloride analogue, on the salt-induced hypertension in inbred Dahl salt-sensitive (SS/jr) rats was assessed. The continuous intracerebroventricular or subcutaneous infusion of benzamil at doses which have no effect when infused systemically was started at the same time or 2 wk after saline was substituted for drinking water, when the rats' blood pressures had become significantly elevated. Within 13 days, drinking saline caused a similar and significant increase in the blood pressures of rats receiving the vehicle intracerebroventricularly and 1 microgram/h of benzamil subcutaneously, which persisted throughout the 4-wk experiment. The intracerebroventricular infusion of 1 or 0.3 microgram/h benzamil, started at the same time the salt challenge was instituted, significantly deterred the increase in blood pressure over 4 wk. The intracerebroventricular, but not the subcutaneous, infusion of benzamil at 0.5 microgram/h arrested the increase in blood pressure in rats that were already hypertensive after 12 days on saline. Within 3 days the pressures in the intracerebroventricular and subcutaneous benzamil groups became significantly different, due to the further increase of the blood pressure in those animals receiving the intracerebroventricular vehicle with subcutaneous benzamil. There was no significant difference in weight gain throughout the experiment or in 24-h urine volumes and urinary Na(+)-to-K+ ratio at days 5 and 12 of benzamil infusion between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic dietary administration of tryptophan prevents the development of deoxycorticosterone acetate salt induced hypertension in rats

1987 ◽  
Vol 65 (5) ◽  
pp. 753-764 ◽  
Author(s):  
Melvin J. Fregly ◽  
Ora E. Lockley ◽  
Judith van der Voort ◽  
Colin Sumners ◽  
William N. Henley
Keyword(s):  
Cardiac Hypertrophy ◽  
Chronic Treatment ◽  
Specific Binding ◽  
Control Level ◽  
Isotonic Saline ◽  
Acute Administration ◽  
Concomitant Treatment ◽  
Deoxycorticosterone Acetate ◽  
Induced Hypertension ◽  
The Brain

Hypertension developed within 3 to 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA) at a dose of 850 μg∙kg−1∙day−1 via Silastic tubes and given isotonic saline to drink. Chronic dietary administration of tryptophan (25 and 50 g/kg of food) to DOCA-treated rats reduced their exaggerated intake of NaCl solution and attenuated the elevation of blood pressure induced by treatment with DOCA alone. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24-h dehydration that is characteristic of DOCA-treated rats. Other tests assessed the responsiveness to the β-adrenergic agonist, isoproterenol. These included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking and chronotropic responses of DOCA-treated rats to acute administration of isoproterenol were unaffected by tryptophan. Responsiveness to angiotensin II (AII) was also tested by assessment of dipsogenic and metabolic responses to acute administration of AII. The increased drinking and tail skin temperature responses to administration of AII, characteristic of DOCA-treated rats, were reduced in a graded fashion by treatment with graded doses of tryptophan. The specific binding of AII to its receptors in membranes from the diencephalon of the brain was increased by treatment with DOCA but was returned to control level by concomitant treatment with tryptophan. The content of serotonin in the mesencephalon of the brain was not changed significantly by treatment with tryptophan, but the content of 5-hydroxyindole acetic acid in the same region increased significantly, suggesting that turnover of serotonin was increased by chronic treatment with tryptophan. The cardiac hypertrophy characteristic of treatment with DOCA was attenuated significantly by chronic treatment with tryptophan, while the low, resting plasma renin activity of the DOCA-treated group was unchanged. These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. It also reduces the hyperresponsiveness to treatment with AII, possibly by decreasing the specific binding of AII to its receptors. It also appears to increase the turnover of serotonin in the brain. Whether either one or all of these is responsible for the antihypertensive effect of tryptophan remains for further study.

Role of vasopressin, catecholamines, and plasma volume in hypertonic saline-induced hypertension

1981 ◽  
Vol 240 (6) ◽  
pp. H827-H831 ◽  
Author(s):  
P. Hatzinikolaou ◽  
H. Gavras ◽  
H. R. Brunner ◽  
I. Gavras
Keyword(s):  
Blood Pressure ◽  
Hypertonic Saline ◽  
Plasma Volume ◽  
Residual Pressure ◽  
Volume Changes ◽  
Beta Adrenoceptor ◽  
Induced Hypertension ◽  
Fluid Load ◽  
Blood Pressures

Elevation of blood pressure induced by an acute sodium and fluid load in the anephric state has been attributed to intravascular fluid volume expansion. The present experiments were designed to study the role of vasopressin and catecholamines in this type of hypertension. Normotensive anephric rats, adrenergically intact or pretreated with alpha- and beta-adrenoceptor blockade, and deoxycorticosterone (DOC)-salt-treated anephric rats, intact or pretreated with alpha- and beta-adrenoceptor blockade, received an infusion of 2 ml containing 3 meq NaCl, followed by intravenous administration of an analogue antagonist of the vasopressor effect of arginine-vasopressin (AVP). Pressure increments induced by hypertonic saline were abolished by an AVP antagonist partly in the adrenergically intact animals (leaving a small residual pressure elevation) and completely in adrenergically blocked animals, which had a larger AVP component. Volumes expansion did not necessarily accompany increase in blood pressure after saline infusion. In fact some DOC-salt-treated animals with the highest blood pressures and norepinephrine levels exhibited contraction of plasma volume. Increments in blood pressure were negatively correlated with plasma volume changes (r = -0.687, P less than 0.05) in these animals and positively with norepinephrine levels in all adrenergically intact animals (r = 0.818, P less than 0.001). It is concluded that the hypertensive response elicited by acute hypertonic saline load is due to vasoconstriction mediated partly by vasopressin and partly by the sympathetic system, which may in some way attenuate the effect of vasopressin.

Chronic exogenous hyperinsulinaemia-induced hypertension in pregnant rats: effect of chronic treatment with l-arginine

2001 ◽  
Vol 100 (6) ◽  
pp. 667-671 ◽  
Author(s):  
Eduardo PODJARNY ◽  
Michael BURSZTYN ◽  
Gloria RASHED ◽  
Sidney BENCHETRIT ◽  
Bernard KATZ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Risk Factor ◽  
Chronic Treatment ◽  
Blood Pressure Response ◽  
Urinary Metabolites ◽  
Pregnant Rats ◽  
Hypertension In Pregnancy ◽  
Induced Hypertension ◽  
In Pregnancy

Recent studies have shown that maternal hyperinsulinaemia is a risk factor for the development of hypertension in pregnancy. Experimentally, pregnant rats with chronic exogenously induced hyperinsulinaemia (P-INS rats) have increased blood pressure at the end of gestation. This is associated with a blunted elevation of the excretion of the urinary metabolites of nitrate (UNOx). In the present study, we aimed to evaluate the mechanism(s) of the increase in blood pressure in this model. Four groups were studied: normal pregnant rats (P rats), P-INS rats, P-INS rats treated with l-arginine (2 g/l in the drinking water) (l-ARG rats) and hyperinsulinaemic virgin rats (V-INS rats). Systolic blood pressure (SBP), UNOx excretion (on ingestion of a controlled low-nitrate diet), urine noradrenaline (norepinephrine) and plasma endothelin levels were evaluated. Rats were killed on day 22 of pregnancy. Five P-INS rats were not killed at this time, in order to measure SBP 30 and 60 days after delivery. Fetal number and fetal body weight were evaluated. At the end of pregnancy, a 10±3% increase in SBP was found in P-INS rats, contrasting with a fall of -15±4% in P rats (P < 0.01). In the l-ARG group at the end of pregnancy, SBP values had fallen by -14±2%, to values comparable with those of P rats. The increase in UNOx excretion was 175±38% in P rats, 106±12% in l-ARG rats and 41±8% in P-INS rats (P < 0.01 compared with P and l-ARG groups). No differences were found in the urinary excretion of noradrenaline or in the plasma levels of endothelin-1 between the pregnant groups. Fetal number was similar in all groups, but fetal body weight was lower for P-INS rats compared with P and l-ARG rats. Thus the blood pressure response to l-arginine strongly suggests that a decrease in NO availability may be the main pathogenic mechanism involved in the development of hypertension in this model.

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