Changes of catecholamines in central and peripheral tissues and in the urines of deoxycorticosterone–salt hypertensive rats

1983 ◽  
Vol 61 (8) ◽  
pp. 888-892 ◽  
Author(s):  
Nguyen T. Buu ◽  
Otto Kuchel ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Hypertensive Rats ◽  
Peripheral Tissues ◽  
Sympathetic Dysfunction ◽  
Salt Hypertension ◽  
Urinary Dopamine ◽  
First Time

The catecholamine concentrations in the urines and in the tissues of the kidney, heart, striatum, and hypothalamus of control rats and rats treated with deoxycorticosterone and salt for 2-week and 5-week periods were measured and compared. In 2-week-treated rats there were no changes in blood pressure and catecholamines. In 5-week-treated rats, the blood pressure increased from 117 ± 5 to 152 ± 5 mmHg (1 mmHg = 0.13 kPa) and there was an increase of urinary dopamine, norepinephrine, and epinephrine. The kidney and heart tissues of the hypertensive rats showed a decrease of norepinephrine while in the hypothalamus all three catecholamines were increased. These data suggest that dopamine and epinephrine may also be involved in the sympathetic dysfunction in deoxycorticosterone–salt hypertension. They demonstrate for the first time an increase of dopamine, norepinephrine, and epinephrine in the hypothalamus of deoxycorticosterone–salt hypertensive rats.

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Afferent Arteriole ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Nephron Loss ◽  
Microsphere Method ◽  
Arteriolar Diameter ◽  
Equal Thickness

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

5-HT2B-receptor antagonist LY-272015 is antihypertensive in DOCA-salt-hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. H944-H952 ◽  
Author(s):  
Stephanie W. Watts ◽  
Gregory D. Fink
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
High Blood Pressure ◽  
Reduce Blood Pressure ◽  
Receptor Expression ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Salt Hypertension

We previously demonstrated a change in the receptors mediating 5-hydroxytryptamine (5-HT)-induced contraction in arteries of deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. Specifically, contraction to 5-HT is mediated primarily by 5-HT2A receptors in arteries from normotensive sham rats and by both 5-HT2A and 5-HT2B receptors in arteries from hypertensive rats. We hypothesized that the 5-HT2B receptor may play a role in maintaining the high blood pressure of DOCA-salt-hypertensive rats, and herein we provide data connecting in vitro and in vivo findings. The endothelium-denuded isolated superior mesenteric artery of DOCA-salt rats displayed a marked increase in maximum contraction to the newly available 5-HT2B-receptor agonist BW-723C86 compared with that of arteries from sham rats, confirming that the 5-HT2B receptor plays a greater role in 5-HT-induced contraction in arteries from DOCA-salt rats. In chronically instrumented rats, the 5-HT2B-receptor antagonist LY-272015 (0.3, 1.0, and 3.0 mg/kg iv at 30-min intervals) was given cumulatively 1 time/wk during 4 wk of continued DOCA-salt treatment. LY-272015 did not reduce blood pressure of the sham-treated rats at any time or dose. However, LY-272015 (1.0 and 3.0 mg/kg) significantly reduced mean blood pressure in a subgroup of week 3 (−20 mmHg) and week 4 DOCA-salt (−40 mmHg) rats that had extremely high blood pressure (mean arterial blood pressure ∼200 mmHg). Blockade of 5-HT2Breceptors by in vivo administration of LY-272015 (3.0 mg/kg) was verified by observing reduced 5-HT-induced contraction in rat stomach fundus, the tissue from which the 5-HT2B receptor was originally cloned. These data support the novel hypothesis that 5-HT2B-receptor expression is induced during the development of DOCA-salt hypertension and contributes to the maintenance of severe blood pressure elevations.

scholarly journals Maternal adaptations to pregnancy in spontaneously hypertensive rats: leptin and ghrelin evaluation

2007 ◽  
Vol 194 (3) ◽  
pp. 611-619 ◽  
Author(s):  
Giuseppina Mattace Raso ◽  
Giuseppe Bianco ◽  
Anna Iacono ◽  
Emanuela Esposito ◽  
Giuseppina Autore ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Leptin Receptor ◽  
Ghrelin Level ◽  
Hypertensive Rats ◽  
Peripheral Tissues ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Complicated Pregnancy ◽  
Plasma Leptin ◽  
First Time

Leptin and/or ghrelin, initially thought to be considered messengers of energy metabolism, are now considered to play a role in normal and complicated pregnancy. In this study, pregnant, spontaneously hypertensive rats (SHR) have been used to evaluate, for the first time, the modification of leptin and ghrelin both at serum and tissue levels. In SHR, we evaluate plasma leptin level and tissue protein expression in both placenta and adipose tissue at the end of gestation (day 20) versus normotensive Wistar–Kyoto (WKY) animals. The expression of functional leptin receptor (Ob-Rb) in peripheral tissues and in the hypothalamus was evaluated. Moreover, we measured plasma ghrelin level and its mRNA expression in the stomach and placenta. SHR strain presented significantly lower plasma leptin levels when compared with those found in pregnant or not WKY controls. Interestingly, in the placenta, leptin gene expression was higher in SHR than normotensive WKY. Moreover, we demonstrated a resistance to the effects of leptin via ‘downregulation’ of hypothalamic receptors in pregnant SHR. Conversely, SHR presented significantly higher ghrelin plasma levels when compared with those found in pregnant or not WKY. However, we observed that ghrelin level in the stomach of SHR did not change during pregnancy, and on the opposite, mRNA ghrelin in the placenta of SHR was lower than that of normotensive rats, suggesting a different production of this hormone in the fetal–placental unit. These data gain further insight into metabolic hormone modifications observed in a model of pre-existing hypertension associated with pregnancy.

Antidiuretic and pressor actions of vasopressin in age-dependent DOCA-salt hypertension

1989 ◽  
Vol 256 (1) ◽  
pp. R138-R145 ◽  
Author(s):  
J. Zicha ◽  
J. Kunes ◽  
M. Lebl ◽  
I. Pohlova ◽  
J. Slaninova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Body Fluids ◽  
Pressure Response ◽  
Fluid Volume ◽  
Brattleboro Rats ◽  
Hypertensive Rats ◽  
Salt Treatment ◽  
Age Dependent ◽  
Salt Hypertension

The role of antidiuretic and pressor effects of vasopressin (VP) in deoxycorticosterone acetate (DOCA)-salt hypertension was studied in young and adult Brattleboro rats. The antidiuretic VP action was a necessary prerequisite for the development of severe DOCA-salt hypertension. The insufficient expansion of extracellular fluid volume in DOCA-salt-treated VP-deficient (DI) rats was associated with the attenuation of their hypertensive response, although they had highly increased blood volume and extracellular sodium. Chronic [deamino]-D-arginine vasopressin supplementation that restored volume and distribution of body fluids in DI rats permitted the full development of DOCA-salt hypertension. Blood pressure response to DOCA-salt treatment was always greater in young than in adult Brattleboro rats (even in animals lacking pressor or both VP effects). In animals in which antidiuretic VP effects were present, the pattern of body fluid response to DOCA-salt treatment was also age dependent. There was a tendency to intravascular expansion in young hypertensive rats, whereas an increase of interstitial fluid volume was found in adult animals. The elimination of VP pressor action lowered systemic resistance much more in adult than in young hypertensive rats. We conclude that 1) in adult but not in young rats antidiuretic VP effects are essential for the occurrence of blood pressure response to DOCA-salt treatment, 2) the restoration of body fluids due to antidiuretic VP action enables the development of hypertension in both age groups of DI rats, and 3) pressor VP effects contribute to the maintenance of hypertension, especially in adult animals.

scholarly journals Effect of a methionine-supplemented diet on the blood pressure of Sprague–Dawley and deoxycorticosterone acetate–salt hypertensive rats

2004 ◽  
Vol 91 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Sophie Robin ◽  
Véronique Maupoil ◽  
Pascal Laurant ◽  
Alain Jacqueson ◽  
Alain Berthelot
Keyword(s):  
Blood Pressure ◽  
Positive Association ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Aortic Constriction ◽  
Deoxycorticosterone Acetate ◽  
Complex Interactions ◽  
Sd Rats ◽  
Salt Hypertension ◽  
Methionine Supplementation

The objectives of the present study were to evaluate the effects of a methionine-supplemented diet on systolic blood pressure (BP) and vasomotor functions in Sprague–Dawley (SD) and deoxycorticosterone acetate (DOCA)–salt hypertensive rats. SD and DOCA rats were fed a normal or a methionine (8 g/kg)-supplemented diet for 10 weeks. Systolic BP was monitored and plasma homocysteine, methionine and cysteine levels were determined at the end of the experiment. Vasoconstriction and vasodilatation of aortic rings were measured. The methionine-supplemented diet induced a greater increase in homocysteinaemia concentration in DOCA rats than in SD rats and an increase in plasma cysteine concentration in DOCA rats. This diet was associated with an increase in systolic BP in SD rats and with a lesser development of DOCA–salt hypertension. An enhanced aortic constriction and a decreased responsiveness to acetylcholine, bradykinin and sodium nitroprusside in the SD rats fed the methionine-rich diet were consistent with the elevated systolic BP. In DOCA rats the increased responsiveness to bradykinin was in accordance with the systolic BP-lowering effect. In conclusion, the methionine-enriched diet cannot simply be considered as model of hyperhomocysteinaemia, since other metabolites and mechanisms seemed to be implicated in these complex interactions. The differential vasopressive effect of the methionine supplementation in SD and DOCA rats, and in particular the lowering of systolic BP obtained with a greater degree of hyperhomocysteinaemia in DOCA rats, suggest that more complex interactions exist between hyperhomocysteinaemia and BP than the simple positive association described previously.

scholarly journals Mycophenolate Improves Brain–Gut Axis Inducing Remodeling of Gut Microbiota in DOCA-Salt Hypertensive Rats

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1199
Author(s):  
Iñaki Robles-Vera ◽  
Néstor de la Visitación ◽  
Manuel Sánchez ◽  
Manuel Gómez-Guzmán ◽  
Rosario Jiménez ◽  
...  
Keyword(s):  
Anaerobic Bacteria ◽  
Immunosuppressive Drug ◽  
Hypertensive Rats ◽  
Gut Dysbiosis ◽  
Paraventricular Nuclei ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Male Wistar Rats ◽  
Host Blood ◽  
First Time

Microbiota is involved in the host blood pressure (BP) regulation. The immunosuppressive drug mofetil mycophenolate (MMF) ameliorates hypertension. The present study analyzed whether MMF improves dysbiosis in mineralocorticoid-induced hypertension. Male Wistar rats were assigned to three groups: untreated (CTR), deoxycorticosterone acetate (DOCA)-salt, and DOCA treated with MMF for 4 weeks. MMF treatment reduced systolic BP, improved endothelial dysfunction, and reduced oxidative stress and inflammation in aorta. A clear separation in the gut bacterial community between CTR and DOCA groups was found, whereas the cluster belonging to DOCA-MMF group was found to be intermixed. No changes were found at the phylum level among all experimental groups. MMF restored the elevation in lactate-producing bacteria found in DOCA-salt joined to an increase in the acetate-producing bacteria. MMF restored the percentage of anaerobic bacteria in the DOCA-salt group to values similar to control rats. The improvement of gut dysbiosis was associated with an enhanced colonic integrity and a decreased sympathetic drive in the gut. MMF inhibited neuroinflammation in the paraventricular nuclei in the hypothalamus. This study demonstrates for the first time that MMF reduces gut dysbiosis in DOCA-salt hypertension models. This effect seems to be related to its capacity to improve gut integrity due to reduced sympathetic drive in the gut associated with reduced brain neuroinflammation.

Inhibitory effect of potassium on blood pressure in DOCA salt hypertension in rats

1981 ◽  
Vol 97 (4) ◽  
pp. 525-532 ◽  
Author(s):  
Hiromichi Suzuki ◽  
Kazuoki Kondo ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Serum Sodium ◽  
Fluid Intake ◽  
Urine Volume ◽  
Plasma Renin ◽  
Hypertensive Rats ◽  
Plasma Aldosterone Concentration ◽  
Salt Hypertension ◽  
Potassium Loading ◽  
Sodium And Potassium

Abstract. The present study was performed to assess the influence of potassium on blood pressure in deoxycorticosterone (DOCA) salt hypertensive rats. The effects of potassium administration on the systolic blood pressure, fluid intake, urine volume, excretion of sodium and potassium, serum sodium and potassium, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were investigated both during the first 2 weeks of development of DOCA salt hypertension and during the next 2 weeks of established DOCA salt hypertension. Potassium administration prevented the development of DOCA salt hypertension and reduced the blood pressure in established DOCA salt hypertension. Fluid intake, urine volume, and excretion of sodium and potassium appeared to be markedly increased in rats treated with potassium. The levels of serum sodium and potassium were unchanged by potassium loading. Both the PRA and PAC which were suppressed in DOCA salt hypertensive rats, were reversed in rats treated by potassium loading. It is suggested that the elevation of blood pressure may be prevented and the increased blood pressure reduced mainly by the diuresis and natriuresis caused by potassium loading.

Failure to demonstrate vasopressor material in salt hypertensive rats

1964 ◽  
Vol 207 (1) ◽  
pp. 152-154 ◽  
Author(s):  
Simon Koletsky ◽  
Walter H. Pritchard
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Sharp Contrast ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Vasopressor Activity

Rats with acute or chronic salt hypertension were assayed for the presence of circulating vasopressor material. The technique consisted of transferring blood from the hypertensive rats to normal recipient rats and measuring the rise in blood pressure of the recipients. The blood of salt hypertensive animals proved to be uniformly devoid of vasopressor activity during the entire course of hypertension. The negative assays matched those obtained with normotensive blood from sham-operated rats and were in sharp contrast to the positive assays in early renal hypertension. The results indicate that salt hypertension is not mediated through a humoral pressor mechanism.

Effect of metformin on the vascular and glucose metabolic actions of insulin in hypertensive rats

2000 ◽  
Vol 278 (5) ◽  
pp. G682-G692 ◽  
Author(s):  
Marta Santuré ◽  
Maryse Pitre ◽  
Nathalie Gaudreault ◽  
André Marette ◽  
André Nadeau ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Whole Body ◽  
Transport Activity ◽  
Hypertensive Rats ◽  
Peripheral Tissues ◽  
Vascular Responses ◽  
Wky Rats

We investigated the long-term effect of metformin treatment on blood pressure, insulin sensitivity, and vascular responses to insulin in conscious spontaneously hypertensive rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and blood flow. Insulin sensitivity was assessed by the euglycemic hyperinsulinemic clamp technique. Two groups of SHR received metformin (100 or 300 mg ⋅ kg− 1 ⋅ day− 1) for 3 wk while another group of SHR and a group of Wistar Kyoto (WKY) rats were left untreated. We found that vasodilation of skeletal muscle and renal vasculatures by insulin is impaired in SHR. Moreover, a reduced insulin sensitivity was detected in vivo and in vitro in isolated soleus and extensor digitorum longus muscles from SHR compared with WKY rats. Three weeks of treatment with metformin improves the whole-body insulin-mediated glucose disposal in SHR but has no blood pressure-lowering effect and no influence on vascular responses to insulin (4 mU ⋅ kg− 1 ⋅ min− 1). An improvement in insulin-mediated glucose transport activity was detected in isolated muscles from metformin-treated SHR, but in the absence of insulin no changes in basal glucose transport activity were observed. It is suggested that part of the beneficial effect of metformin on insulin resistance results from a potentiation of the hormone-stimulating effect on glucose transport in peripheral tissues (mainly skeletal muscle). The results argue against a significant antihypertensive or vascular effect of metformin in SHR.

Reduced contractile sensitivity and vasopressin receptor affinity in DOCA-salt hypertension

1992 ◽  
Vol 262 (6) ◽  
pp. H1752-H1758 ◽  
Author(s):  
C. S. Bockman ◽  
W. B. Jeffries ◽  
W. A. Pettinger ◽  
P. W. Abel
Keyword(s):  
Blood Pressure ◽  
Mesenteric Arteries ◽  
Elevated Blood Pressure ◽  
Vasopressin Receptor ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Receptor Affinity ◽  
Receptor Agonists ◽  
Salt Hypertension ◽  
Vasopressin Receptors

The affinity of vascular vasopressin receptors was studied to determine its role in altered vascular contractile sensitivity in deoxycorticosterone acetate (DOCA)-salt hypertension. Ring segments of rat mesenteric arteries were used to study vascular vasopressin receptors. Male Wistar rats were given subcutaneous injections of DOCA and 1% NaCl in the drinking water. Mesenteric arteries from hypertensive rats had a reduced contractile sensitivity to arginine vasopressin (AVP) and lysine vasopressin (LVP). The order of potency of vasopressin receptor agonists (AVP greater than LVP greater than oxytocin) was the same in arteries from hypertensive compared with normotensive animals. The affinity of the vasopressin receptor antagonist [deamino-Pen1,O-Me-Tyr2,Arg8] vasopressin, and the affinities of the vasopressin receptor agonists AVP and LVP were not altered during developing DOCA-salt hypertension. There was no change in contractile sensitivity to norepinephrine and KCl in arteries from hypertensive rats. The reduced vasopressin contractile sensitivity is not due to a change in vasopressin receptor affinity but may be a compensatory response to elevated blood pressure. These data suggest that increased vascular sensitivity does not contribute to elevated blood pressure during the developing stage of DOCA-salt hypertension.

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