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.

Role of Autonomic Nervous System in Maintenance of Cerebral and Renal Hypertension

1957 ◽  
Vol 188 (2) ◽  
pp. 371-374 ◽  
Author(s):  
Sol Rothman ◽  
Douglas R. Drury
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Renal Hypertension ◽  
The Other ◽  
Peripheral Vasculature ◽  
Blood Pressures ◽  
Sympathetic Nervous ◽  
Blood Pressure Responses

The blood pressure responses to various drugs were investigated in renal hypertensive, cerebral hypertensive and normotensive rabbits. Hexamethonium bromide and Dibenamine reduced the blood pressures of renal and cerebral hypertensives. Effects in the normal were insignificant. The cerebral hypertensive's blood pressure was slightly affected by benzodioxane. Blood pressure was not reduced at all in the other groups. Blood pressure of the renal hypertensive rabbit was greatly reduced by Veriloid and dihydroergocornine. Blood pressures of cerebral and normal animals were affected to a lesser degree. The results suggest that maintenance of hypertension in the cerebral hypertensive rabbit depends on an overactive sympathetic nervous system, possibly due to the release of medullary pressor centers from inhibitory impulses originating in higher centers; whereas, the maintenance of hypertension in the renal hypertensive rabbit may be attributed to an increased reactivity of the peripheral vasculature to a normal sympathetic tone.

Physical exercise and blood pressure with reference to the angiotensinogen M235T polymorphism

2002 ◽  
Vol 10 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Rainer Rauramaa ◽  
Raimo Kuhanen ◽  
Timo A. Lakka ◽  
Sari B. Väisänen ◽  
Pirjo Halonen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Reference Group ◽  
Controlled Trial ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Blood Pressures ◽  
Agt Gene ◽  
M235t Polymorphism

We investigated the role of the angiotensinogen (AGT) gene M235T polymorphism in determining blood pressure (BP) response to moderate intensity exercise in a 6-yr randomized controlled trial in 140 middle-aged men. Sitting, supine, and standing blood pressures were measured annually. Of the randomized men, 86% participated in the trial for 6 yr. Submaximal cardiorespiratory fitness increased by 16% in the exercise group. In the M homozygotes, sitting systolic BP decreased by 1.0 mmHg in the exercise but increased by 14.6 mmHg in the reference group ( P = 0.007 for net effect). Sitting and supine diastolic BP decreased by 6.2 and 3.3 mmHg in the exercise but increased by 2.8 and 3.2 mmHg in the reference group ( P = 0.026 and 0.024 for net effects), respectively. Regular moderate intensity exercise attenuates aging-related increase in systolic BP and decreases diastolic BP among the M homozygotes of the AGT gene M235T polymorphism.

Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region

1999 ◽  
Vol 276 (1) ◽  
pp. H63-H70 ◽  
Author(s):  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Hypertonic Saline ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Air Jet ◽  
Artificial Cerebrospinal Fluid ◽  
Induced Hypertension ◽  
Chronic Infusion

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.

scholarly journals Role of myosin light chain kinase in regulation of basal blood pressure and maintenance of salt-induced hypertension

2011 ◽  
Vol 301 (2) ◽  
pp. H584-H591 ◽  
Author(s):  
Wei-Qi He ◽  
Yan-Ning Qiao ◽  
Cheng-Hai Zhang ◽  
Ya-Jing Peng ◽  
Chen Chen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Myosin Light Chain ◽  
Vascular Tone ◽  
Induced Hypertension ◽  
Basal Blood Pressure ◽  
Muscle Myosin

Vascular tone, an important determinant of systemic vascular resistance and thus blood pressure, is affected by vascular smooth muscle (VSM) contraction. Key signaling pathways for VSM contraction converge on phosphorylation of the regulatory light chain (RLC) of smooth muscle myosin. This phosphorylation is mediated by Ca2+/calmodulin-dependent myosin light chain kinase (MLCK) but Ca2+-independent kinases may also contribute, particularly in sustained contractions. Signaling through MLCK has been indirectly implicated in maintenance of basal blood pressure, whereas signaling through RhoA has been implicated in salt-induced hypertension. In this report, we analyzed mice with smooth muscle-specific knockout of MLCK. Mesenteric artery segments isolated from smooth muscle-specific MLCK knockout mice (MLCKSMKO) had a significantly reduced contractile response to KCl and vasoconstrictors. The kinase knockout also markedly reduced RLC phosphorylation and developed force. We suggest that MLCK and its phosphorylation of RLC are required for tonic VSM contraction. MLCKSMKO mice exhibit significantly lower basal blood pressure and weaker responses to vasopressors. The elevated blood pressure in salt-induced hypertension is reduced below normotensive levels after MLCK attenuation. These results suggest that MLCK is necessary for both physiological and pathological blood pressure. MLCKSMKO mice may be a useful model of vascular failure and hypotension.

Haemodynamic Changes Associatedc with Obesity and High Blood Pressure in Crats with Ventromedial Hypothalamic Lesions

1980 ◽  
Vol 59 (s6) ◽  
pp. 397s-399s ◽  
Author(s):  
E. Reisin ◽  
D. H. Suarez ◽  
E. D. Frohlich
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
High Blood Pressure ◽  
Plasma Volume ◽  
Mild Hypertension ◽  
Male Rats ◽  
Volume Changes ◽  
Hypothalamic Lesions ◽  
Haemodynamic Changes ◽  
Mild Obesity

1. The haemodynamic and plasma volume changes associated with obesity and high blood pressure were studied in nine male rats with electrolytic ventromedial hypothalamic lesions and their paired sham-operated controls. Body weight and arterial pressure were greater in the rats with ventromedial hypothalamic lesions (565 ± 16 vs 462 ± 14 g, P<0.001; 128 ± 3 vs 118 ± 3 mmHg, P<0.05, respectively). Cardiac output was slightly elevated, and that portion of cardiac output distributed to the kidneys was reduced (P<0.001). Plasma volume was contracted in the rats with ventromedial hypothalamic lesions (21.0 ± 0.1 vs 2.8 ± 0.1 ml/100 g, P<0.001). 2. The haemodynamic characteristics of rats in which obesity and mild hypertension have been induced by electrolytic ventromedial hypothalamic lesion are similar to mild obesity essential hypertension in men.

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 Genetic and genomic evidence for an important role of the Na+/H+ exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension

2019 ◽  
Vol 51 (4) ◽  
pp. 97-108 ◽  
Author(s):  
Xiao C. Li ◽  
Xiaowen Zheng ◽  
Xu Chen ◽  
Chunling Zhao ◽  
Dongmin Zhu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Proximal Tubules ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Blood Pressure Homeostasis ◽  
Induced Hypertension ◽  
Basal Blood Pressure

The sodium (Na+)/hydrogen (H+) exchanger 3 (NHE3) and sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) are two of the most important Na+ transporters in the proximal tubules of the kidney. On the apical membrane side, NHE3 primarily mediates the entry of Na+ into and the exit of H+ from the proximal tubules, directly and indirectly being responsible for reabsorbing ~50% of filtered Na+ in the proximal tubules of the kidney. On the basolateral membrane side, Na+/K+-ATPase serves as a powerful engine driving Na+ out of, while pumping K+ into the proximal tubules against their concentration gradients. While the roles of NHE3 and Na+/K+-ATPase in proximal tubular Na+ transport under in vitro conditions are well recognized, their respective contributions to the basal blood pressure regulation and angiotensin II (ANG II)-induced hypertension remain poorly understood. Recently, we have been fortunate to be able to use genetically modified mouse models with global, kidney- or proximal tubule-specific deletion of NHE3 to directly determine the cause and effect relationship between NHE3, basal blood pressure homeostasis, and ANG II-induced hypertension at the whole body, kidney and/or proximal tubule levels. The purpose of this article is to review the genetic and genomic evidence for an important role of NHE3 with a focus in the regulation of basal blood pressure and ANG II-induced hypertension, as we learned from studies using global, kidney- or proximal tubule-specific NHE3 knockout mice. We hypothesize that NHE3 in the proximal tubules is necessary for maintaining basal blood pressure homeostasis and the development of ANG II-induced hypertension.

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.

Sign in / Sign up

Export Citation Format

Share Document