scholarly journals Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension

2010 ◽  
pp. 997-1009 ◽  
Author(s):  
S Hojná ◽  
J Kuneš ◽  
J Zicha
Keyword(s):  
Blood Pressure ◽  
Pressure Control ◽  
Brain Regions ◽  
No Synthase ◽  
Inos Expression ◽  
Sympathetic Tone ◽  
No Production ◽  
Adult Rats ◽  
Induced Hypertension ◽  
Salt Hypertension

Both brain and peripheral nitric oxide (NO) play a role in the control of blood pressure and circulatory homeostasis. Central NO production seems to counteract angiotensin II-induced enhancement of sympathetic tone. The aim of our study was to evaluate NO synthase (NOS) activity and protein expression of its three isoforms – neuronal (nNOS), endothelial NOS (eNOS) and inducible (iNOS) – in two brain regions involved in blood pressure control (diencephalon and brainstem) as well as in the kidney of young adult rats with either genetic (12-week-old SHR) or saltinduced hypertension (8-week-old Dahl rats). We have demonstrated reduced nNOS and iNOS expression in brainstem of both hypertensive models. In SHR this abnormality was accompanied by attenuated NOS activity and was corrected by chronic captopril treatment which prevented the development of genetic hypertension. In salt hypertensive Dahl rats nNOS and iNOS expression was also decreased in the diencephalon where neural structures important for salt hypertension development are located. As far as peripheral NOS activity and expression is concerned, renal eNOS expression was considerably reduced in both genetic and salt-induced hypertension. In conclusions, we disclosed similar changes of NO system in the brainstem (but not in the diencephalon) of rats with genetic and salt-induced hypertension. Decreased nNOS expression was associated with increased blood pressure due to enhanced sympathetic tone.

scholarly journals Hypertension in Prenatally Undernourished Young-Adult Rats Is Maintained by Tonic Reciprocal Paraventricular–Coerulear Excitatory Interactions

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3568
Author(s):  
Bernardita Cayupe ◽  
Carlos Morgan ◽  
Gustavo Puentes ◽  
Luis Valladares ◽  
Héctor Burgos ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Young Adult ◽  
Binding Sites ◽  
Systolic Pressure ◽  
Adult Rats ◽  
Excitatory Pathways ◽  
Induced Hypertension ◽  
Prenatal Undernutrition ◽  
Number Of Cells

Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular–coerulear excitatory interactions in prenatally undernourished young-adult rats.

Abstract P060: Angiotensin AT1A Receptors on Vasopressin-Expressing Cells are Dispensable for DOCA-salt Hypertension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jeremy A Sandgren ◽  
Danny W Linggonegoro ◽  
Kristin E Claflin ◽  
Nicole A Pearson ◽  
Gary L Pierce ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Control ◽  
Specific Activity ◽  
Fluorescent Microscopy ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Fluorescent Reporter ◽  
Significant Difference ◽  
Low Renin Hypertension ◽  
Salt Hypertension

Increased blood pressure in the deoxycorticosterone acetate (DOCA)-salt model of low-renin hypertension is correlated with increased vasopressin (AVP) secretion, and is sensitive to inhibition of the brain renin-angiotensin system (RAS). Further, AVP-deficient Brattleboro rats are largely resistant to DOCA-salt hypertension. These findings lead us to hypothesize a role for AT1A receptors localized to AVP-expressing neurons in the control of AVP secretion, specifically in low-renin hypertension. Blood pressure was assessed via tail-cuff plesthysmography and total daily AVP secretion assessed via urine copeptin in mice with specific disruption of the AT1A gene in AVP-expressing cells (AVP-Cre x AT1Aflox/flox mice, “KO”) under both baseline and DOCA-salt treatment conditions. Specific activity of Cre-recombinase within the paraventricular and supraoptic nuclei of AVP-Cre transgenic mice was confirmed by fluorescent microscopy in brain sections from mice expressing a conditional fluorescent reporter (AVP-Cre x ROSA-stopflox-tdTomato mice). At baseline, AVP secretion (via urine copeptin) trended downward with large variation (control n=17, 363±182 vs KO n=5, 33±11 pg/day; p>0.05) but there was no significant difference in blood pressure (control n=27, 107±1.3 vs KO n=12, 111±2.2 mmHg; p>0.05) compared to littermate controls. In response to DOCA-salt, blood pressure (control n=23, +10.35±2.1 vs KO n=8, +12.91±2.0; p>0.05), urine output (control n=23, +12.65±0.8 vs KO n=9, +12.73±1.5 g/day; p>0.05), and fluid intake (control n=23, +16.17±1.3 vs KO n=9, +14.83±2.5 mL/day; p>0.05) increased normally in KO mice. Preliminary findings indicate normal or possibly exaggerated urine copeptin levels in KO mice following DOCA-salt, and an exaggerated AVP release in response to increasing serum osmolality. Collectively, these data suggest that AT1A receptors on AVP expressing cells are required to mediate baseline secretion of AVP, but that these receptors are dispensable for DOCA-salt mediated increases in circulating AVP and blood pressure.

scholarly journals Contribution of captopril thiol group to the prevention of spontaneous hypertension

2007 ◽  
pp. S41-S48
Author(s):  
O Pecháňová
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Ace Inhibitors ◽  
Thiol Group ◽  
No Synthase ◽  
Spontaneous Hypertension ◽  
Cgmp Level ◽  
Control Group ◽  
No Production ◽  
Enalapril Group

We aimed to compare the effect of angiotensin converting enzyme (ACE) inhibitors captopril (containing thiol group) and enalapril (without thiol group) on the development of spontaneous hypertension and to analyze mechanisms of their actions, particularly effects on oxidative stress and NO production. Six-week-old SHR were divided into three groups: control, group receiving captopril (50 mg/kg/day) or enalapril (50 mg/kg/day) for 6 weeks. At the end of experiment, systolic blood pressure (SBP) increased by 41 % in controls. Both captopril and enalapril prevented blood pressure increase, however, SBP in the captopril group (121+/-5 mmHg) was significantly lower than that in the enalapril group (140+/-5 mmHg). Concentration of conjugated dienes in the aorta was significantly lower in the captopril group compared to the enalapril group. Captopril and enalapril increased NO synthase activity in the heart and aorta to the similar level. Neither captopril nor enalapril was, however, able to increase the expression of eNOS. Both ACE inhibitors increased the level of cGMP. However, cGMP level was significantly higher in the aorta of captopril group. We conclude that captopril, beside inhibition of ACE, prevented hypertension by increasing NO synthase activity and by simultaneous decrease of oxidative stress which resulted in increase of cGMP concentration.

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.

The Influence of Neonatal Treatment with Guanethidine on the Development of Isolation-Induced Hypertension in Adult Rats

1983 ◽  
Vol 65 (5) ◽  
pp. 469-474 ◽  
Author(s):  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Wistar Rats ◽  
Adult Rats ◽  
Male And Female ◽  
Neonatal Treatment ◽  
Induced Hypertension ◽  
Female Wistar Rats ◽  
Sympathetic Nervous

1. Rats housed individually in glass metabolism cages develop hypertension. Since previous experiments have provided some evidence for the involvement of the sympathetic nervous system in the maintenance of the hypertension, the present work was designed to explore the possible involvement of the sympathetic nervous system in the genesis of isolation-induced hypertension. 2. Male and female Wistar rats were treated neonatally with guanethidine, with a protocol designed to produce an extensive peripheral sympathectomy; control rats received saline. 3. The effects of isolation on systolic blood pressure and fluid and electrolyte balances were studied when the rats were mature. 4. Guanethidine-treated rats did not develop hypertension in response to isolation whereas control rats did. 5. There were no significant differences between the fluid and electrolyte balances of the guanethidine-treated rats compared with controls throughout the period of isolation. 6. It is concluded that a fully functional sympathetic nervous system is required for the development of isolation-induced hypertension, but its involvement is not through a modulation of renal function.

scholarly journals INTRAVENOUS LABETALOL VERSUS ORAL NIFEDIPINE FOR ACUTE BLOOD PRESSURE CONTROL IN SEVERE PREGNANCY-INDUCED HYPERTENSION- A RANDOMISED TRIAL

2017 ◽  
Vol 6 (92) ◽  
pp. 6578-6582
Author(s):  
Ramprasad Dey ◽  
Arunima Mukhopadhyay ◽  
Subhash Chandra Biswas ◽  
Siuli Chanda Chakrabarti ◽  
Joyeeta Monda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Control ◽  
Randomised Trial ◽  
Pressure Control ◽  
Pregnancy Induced Hypertension ◽  
Induced Hypertension

scholarly journals Salt-induced hypertension in Dahl salt-resistant and salt-sensitive rats with NOS II inhibition

1999 ◽  
Vol 277 (2) ◽  
pp. H732-H739 ◽  
Author(s):  
M. Audrey Rudd ◽  
Maria Trolliet ◽  
Susan Hope ◽  
Anne Ward Scribner ◽  
Geraldine Daumerie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
No Synthase ◽  
No Production ◽  
Induced Hypertension ◽  
Blood Pressures ◽  
Diameter Change ◽  
Inducible Nos ◽  
Tail Cuff

Although recent evidence suggests that reduced nitric oxide (NO) production may be involved in salt-induced hypertension, the specific NO synthase (NOS) responsible for the conveyance of salt sensitivity remains unknown. To determine the role of inducible NOS (NOS II) in salt-induced hypertension, we treated Dahl salt-resistant (DR) rats with the selective NOS II inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) for 12 days. Tail-cuff systolic blood pressures rose 29 ± 6 and 42 ± 8 mmHg in DR rats given 150 and 300 nmol AMT/h, respectively ( P < 0.01, 2-way ANOVA) after 7 days of 8% NaCl diet. We observed similar results with two other potent selective NOS II inhibitors, S-ethylisourea (EIT) and N-[3-(aminomethyl)benzyl]acetamidine hydrochloride (1400W). Additionally, AMT effects were independent of alterations in endothelial function as assessed by diameter change of mesenteric arterioles in response to methacholine using videomicroscopy. We, therefore, conclude from these data that NOS II is important in salt-induced hypertension.

scholarly journals Exposure to zinc deficiency in fetal and postnatal life determines nitric oxide system activity and arterial blood pressure levels in adult rats

2010 ◽  
Vol 104 (3) ◽  
pp. 382-389 ◽  
Author(s):  
Analía Tomat ◽  
Rosana Elesgaray ◽  
Valeria Zago ◽  
Héctor Fasoli ◽  
Andrea Fellet ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Systolic Blood Pressure ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
No Synthase ◽  
Male Offspring ◽  
Fetal Life ◽  
Adult Rats ◽  
System Activity

We had previously shown that prenatal exposure to Zn-deficient diets induces an increase in blood pressure and impairs renal function in adult rats. The aim of the present study was to investigate if moderate Zn restriction during early growth periods, fetal life and lactation would induce impairment in the vascular and renal NO system and alterations in plasma lipid profile. We also investigated if these effects persisted into adult life, even when a Zn-replete diet was provided after weaning. Pregnant rats were fed control (30 parts per million (ppm)) or low (8 ppm) Zn diets throughout gestation up to weaning. Afterwards, male offspring from low-Zn mothers were assigned to low- or control-Zn diets during 60 d. Male offspring from control mothers were fed a control diet. Animals exposed to Zn restriction showed low birth weight, increased systolic blood pressure and serum TAG levels, and decreased glomerular filtration rate in adulthood. Zn restriction induced a decrease in vascular and renal NO synthase activity and a reduced expression of the endothelial NO synthase isoform in aorta. A control-Zn diet during post-weaning growth returned TAG levels to normal but was unsuccessful in normalising systolic blood pressure, glomerular filtration rate or NO system activity in Zn-deficient offspring. Zn restriction during fetal life, lactation and/or post-weaning growth induced alterations in the vascular and renal NO system and in lipid metabolism that could contribute to the programming of hypertension and renal dysfunction in adulthood.

Medullipin System of Blood Pressure Control

Physiology ◽  
1990 ◽  
Vol 5 (6) ◽  
pp. 241-244 ◽  
Author(s):  
EE Muirhead
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Blood Pressure Control ◽  
Pressure Control ◽  
Suppressive Effect ◽  
Interstitial Cells ◽  
Sympathetic Tone ◽  
Renal Papilla ◽  
The Central Nervous System

Renomedullary interstitial cells of renal papilla secrete medullipin I, which is conveyed to the liver and converted to medullipin II, a vasodilator that suppresses sympathetic tone, causes diuresis-natriuresis, and has a suppressive effect on the central nervous system. These are opposite effects to those of renin-angiotensin.

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