Influence of Sodium on Experimental Renovascular Hypertension in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 149s-151s ◽  
Author(s):  
C. M. Taquini ◽  
A. Gallo ◽  
N. Basso ◽  
A. C. Taquini
Keyword(s):  
Plasma Renin Activity ◽  
Control Period ◽  
Plasma Renin ◽  
Diet Group ◽  
Renin Activity ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Group 2 ◽  
Group 1

1. Rats on normal sodium diet (group 1) and on chronically maintained low sodium diet (group 2) were studied during a control period, after clipping the renal artery (two-kidney, one-clip hypertension) and after nephrectomy (one-kidney, one-clip hypertension). 2. The low sodium diet neither prevented the development nor changed the severity of two-kidney, one-clip hypertension, and the latter was not accompanied by an increase in plasma renin activity. 3. After nephrectomy arterial pressure further increased and plasma renin activity decreased in group 1, and both remained unchanged in group 2. 4. Blood volume was the same in both groups 10 days before and 10 days after nephrectomy. 5. Sodium does not seem to be ‘necessary’ in the two-kidney, one-clip hypertension although it may play an enhancing role in the one-kidney model.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

Evidence that the Acute Cardiovascular Response to Isoprenaline is Partly Mediated via Renin Release

1979 ◽  
Vol 57 (1) ◽  
pp. 13-18 ◽  
Author(s):  
G. H. Anderson
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Infusion Rate ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. The possible effect of the increased plasma renin activity induced by β−adrenoreceptor stimulation in supporting arterial pressure has been studied in five normal subjects on a diet of 100 mmol of sodium/day for 4 days or 40 mmol of sodium/day for 4 days by infusing isoprenaline at 1·0, 2·0 or 3·0 μg min−170 kg−1, each for 1 h with 45 min between each infusion rate. During the last 30 min of each isoprenaline dose, the angiotensin II analogue [Sar1, Ala8]angiotensin II (saralasin) was infused. 2. Isoprenaline significantly (at least P <0·05) increased the pulse rate, systolic arterial pressure and plasma renin activity; the diastolic blood pressure decreased but the mean arterial pressure did not change. Saralasin administered to subjects on the 100 mmol of sodium/day diet significantly (at least P < 0·05) lowered mean arterial pressure at the two highest isoprenaline infusion rates. 3. With patients on a low sodium diet, saralasin lowered mean arterial pressure at all three isoprenaline infusion rates. On the low sodium diet the fall in mean arterial pressure caused by saralasin was significantly greater (P < 0·05) at the isoprenaline infusion rate of 3·0 μg min−1 70 kg−1 than at the infusion rate of 1·0 μg min−1 70 kg−1. The change in mean arterial pressure with saralasin before and during isoprenaline infusion on both diets was significantly correlated (r = −0·39, n = 38, P < 0·01) with the plasma renin activity measured immediately before saralasin infusion. 4. It is concluded that during β−adrenoreceptor stimulation the increased plasma renin activity (acting through angiotensin) supports arterial pressure.

Effects of AVP and DDAVP on plasma renin activity and electrolyte excretion in conscious dogs

1979 ◽  
Vol 236 (1) ◽  
pp. F66-F70 ◽  
Author(s):  
M. D. Johnson ◽  
L. B. Kinter ◽  
R. Beeuwkes
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Renin Activity ◽  
Electrolyte Excretion ◽  
Indwelling Catheters ◽  
Urinary Osmolality ◽  
Low Sodium Diet ◽  
Low Sodium

Uninephrectomized adult female dogs with chronic indwelling catheters were maintained on a low sodium diet and studied without anesthesia. Following hydration with 3% dextrose, an intravenous infusion of either arginine vasopressin (AVP) or of 1-desamino-8-D-arginine vasopressin (DDAVP) was begun. The dose was calculated to achieve a near maximal physiological plasma concentration of AVP, or an equimolar concentration of DDAVP. Both AVP and DDAVP increased urinary osmolality from less than 60 to over 800 mosmol/kg H2O within 1 h. AVP infusion increased mean arterial pressure and renal electrolyte excretion and decreased heart rate and plasma renin activity (PRA), while DDAVP was without effect on these parameters. AVP infused into the renal artery at doses which did not alter systemic pressure and heart rate caused kaliuresis and reduced PRA. We conclude that the AVP-induced inhibition of renin secretion and increase in renal electrolyte excretion are not secondary to increased tubular permeability to water, but must represent a more specific action of AVP which is not shared by DDAVP.

Effects of sodium intake and aldosterone on the renal pressure-natriuresis

1988 ◽  
Vol 254 (5) ◽  
pp. F697-F703 ◽  
Author(s):  
S. B. Harrap ◽  
S. A. Clark ◽  
R. Fraser ◽  
A. Towrie ◽  
A. J. Brown ◽  
...  
Keyword(s):  
Plasma Aldosterone ◽  
Sodium Reabsorption ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Group 3 ◽  
Group 2 ◽  
Pressure Natriuresis ◽  
Group 1

To study the effects of dietary sodium and plasma aldosterone on pressure-natriuresis (PN) we examined six groups of adult, male Sprague-Dawley rats. Group 1 received normal-sodium diet, group 2 high-sodium diet, and group 3 low-sodium diet for 3 wk; group 4 was given low sodium for 3 wk then high sodium for 3 wk; groups 5 and 6 received high sodium for 3 wk but during the 3rd wk were also given aldosterone by subcutaneous infusion to mimic the plasma aldosterone seen in groups 1 and 3, respectively. After the diets, rats were killed, and urinary sodium excretion, glomerular filtration rate (GFR), and calculated tubular sodium reabsorption (FRNa) were measured during stepwise increases in perfusion pressure in isolated perfused kidneys from each group. No significant differences in blood pressure were seen between any of the groups. The PN curves for groups 2 and 3 were significantly different (P less than 0.001) and shifted to the left and right of group 1, respectively. These shifts appeared to be the result of significant (P less than 0.001) differences in FRNa rather than changes in GFR. PN was not significantly different in groups 4 and 2, indicating that the effects of low-sodium diet were reversible. The infusion of aldosterone in groups 5 and 6 was associated with modest and significant (P less than 0.001) shifts, respectively, of the PN curve to the right of the curve of rats in group 2. In group 6 this shift appeared to be due to significant (P less than 0.001) changes in FRNa, so as to resemble that seen in low-sodium rats of group 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion

1987 ◽  
Vol 253 (1) ◽  
pp. R179-R185
Author(s):  
E. Gotoh ◽  
K. Murakami ◽  
T. D. Bahnson ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Renin Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Head Up Tilt ◽  
Dorsal Raphé

To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

Plasma renin activity and forearm blood flow in paraplegic humans

1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Forearm Blood Flow ◽  
Control Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Body ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

Hypotensive effect of [Sar1,Thr8]angiotensin II in spontaneously hypertensive sodium-depleted rats

1978 ◽  
Vol 234 (4) ◽  
pp. H447-H453
Author(s):  
H. Munoz-Ramirez ◽  
M. C. Khosla ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Normal Diet ◽  
Spontaneously Hypertensive ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Angiotensin Ii Antagonist

Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. The angiotensin antagonist also lowered blood pressure of young and mature SH rats receiving a normal diet. Deoxycorticosterone acetate (DOCA) plus saline reversed the hypotensive effect of [Saru,Thr8]angiotensin II in young SH rats, but did not do so in mature SH rats. Plasma renin activity (PRA) was not significantly changed by anesthesia. Furosemide or the low-sodium diet significantly increased PRA in young and mature SH rats. In contrast, DOCA plus saline significantly reduced PRA in both young and mature SH rats. However, there was no correlation between PRA and the action of the angiotensin II antagonist. These data suggest that the renin-angiotensin system is involved in genetic hypertension.

Comparative analysis of direct renin levels and plasma renin activity for the purpose of monitoring the patients with congenital adrenal cortical hyperplasia

2013 ◽  
Vol 59 (5) ◽  
pp. 9-15
Author(s):  
T A Ionova ◽  
G S Kolesnikova ◽  
N Iu Kalinchenko
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Diagnostic Value ◽  
Russian Language ◽  
Renin Activity ◽  
Research Centre ◽  
Endocrine Organs ◽  
High Prevalence ◽  
Group 2 ◽  
The Relationship

The high prevalence of diseases associated with the disturbances in the renin-angiotensin-aldosterone system (RAAS) including those affecting the children dictates the necessity of the development and application of highly specific, accurate, and sensitive indices. One of them widely used at present is plasma renin activity (PRA). Meanwhile, foreign researchers have demonstrated significant correlation between PRA and direct renin concentration that can be determined by a technically simpler and readily available method. We are unaware of the studies with the application of this approach reported in the Russian-language publications. The present work was designed to consider the possibility of using direct rennin levels and PRA for monitoring health conditions of the children presenting with congenital adrenal cortical hyperplasia. PRA and direct rennin concentrations were determined with the use of the relevant assay kits in 72 patients admitted to the Pediatric Department of Endocrinological Research Centre. Group 1 was comprised of 44 patients presenting with congenital adrenal cortical hyperplasia (CAH), group 2 consisted of 28 patients with the presumably unaffected adrenal function. Direct rennin concentrations and PRA are known to have virtually identical diagnostic value, i.e. they can equally well be used to diagnose disorders of RAAS functions including those in the patients with CAH. However, the measurement of direct rennin permits to more precisely detect hyperaldosteronism and identify children exhibiting symptoms of mineralocorticoid overdose. The patients with the supposedly normal functioning adrenal glands were also found to show high percentage of abnormal PRA values and direct rennin levels which suggests the relationship between the functions of RAAS and other endocrine organs.

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