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.

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.

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.

Effect of caffeine treatment of plasma renin activity and angiotensin I concentrations in rats on a low sodium diet

Life Sciences ◽  
1993 ◽  
Vol 52 (10) ◽  
pp. 883-890 ◽  
Author(s):  
Ching-Jiunn Tseng ◽  
Chia-Jen Kuan ◽  
Hsin Chu ◽  
Che-Se Tung
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin I ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Caffeine Treatment

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

Renal Denervation Prevents Sodium Retention and Hypertension in Salt-Sensitive Rabbits with Genetic Baroreflex Impairment

1996 ◽  
Vol 90 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Marta Weinstock ◽  
Elena Gorodetsky ◽  
Ronald Kalman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Group I ◽  
Group Ii

1. Rabbits with a genetic impairment in baroreflex control of heart rate become hypertensive on a high salt diet. The present study determined the effect of bilateral renal denervation on blood pressure and sodium balance after salt loading (four times normal intake; 28–36 mEq NaCl/day) in normotensive rabbits with high (Group I) and low (Group II) baroreflex sensitivity, respectively. 2. Eight rabbits in each group were denervated or sham-denervated 1 week before commencement of the high salt diet. Before operation, the two groups differed only in the gain of their cardiac baroreflex (Group I, −6.4 ± 0.4 beats min−1 mmHg−1; Group II, −3.2 ± 0.15 beats min−1 mmHg−1). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and heart rate fell significantly in response to the high salt. In Group II sham-denervated rabbits, mean arterial pressure increased by 10.6 ± 1.2 mmHg, and heart rate and plasma renin activity remained unchanged. Their cumulative Na+ retention and weight gain was more than twice that of Group I sham-denervated rabbits. 4. Renal denervation decreased plasma renin activity in both groups to <1 pmol Ang I h−1 ml−1, lowered cumulative Na+ retention from 102 ± 4 to 35 ± 5 mEq (P<0.01) and completely prevented the increase in mean arterial pressure in response to high salt in Group II. 5. The results suggest that Group II rabbits retain salt and fluid in response to their diet because of an abnormality in their control of renal nerve activity, possibly via vagal afferents. This results in blood pressure elevation because of an inability to lower peripheral resistance and heart rate in response to the increase in cardiac output. 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension.

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.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

scholarly journals Angiotensin II utilizes Janus kinase 2 in hypertension, but not in the physiological control of blood pressure, during low-salt intake

2011 ◽  
Vol 301 (4) ◽  
pp. R1169-R1176 ◽  
Author(s):  
Amy K. L. Banes-Berceli ◽  
Hind Al-Azawi ◽  
Daniel Proctor ◽  
Harvey Qu ◽  
Dominic Femminineo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Janus Kinase ◽  
Ang Ii ◽  
Physiological Control ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Low Salt

Janus kinase (JAK) 2 is activated by ANG II in vitro and in vivo, and chronic blockade of JAK2 by the JAK2 inhibitor AG-490 has been shown recently to attenuate ANG II hypertension in mice. In this study, AG-490 was infused intravenously in chronically instrumented rats to determine if the blunted hypertension was linked to attenuation of the renal actions of ANG II. In male Sprague-Dawley rats, after a control period, ANG II at 10 ng·kg−1·min−1 was infused intravenously with or without AG-490 at 10 ng·kg−1·min−1 iv for 11 days. ANG II infusion (18 h/day) increased mean arterial pressure from 91 ± 3 to 168 ± 7 mmHg by day 11. That response was attenuated significantly in the ANG II + AG-490 group, with mean arterial pressure increasing only from 92 ± 5 to 127 ± 3 mmHg. ANG II infusion markedly decreased urinary sodium excretion, caused a rapid and sustained decrease in glomerular filtration rate to ∼60% of control, and increased renal JAK2 phosphorylation; all these responses were blocked by AG-490. However, chronic AG-490 treatment had no effect on the ability of a separate group of normal rats to maintain normal blood pressure when they were switched rapidly to a low-sodium diet, whereas blood pressure fell dramatically in losartan-treated rats on a low-sodium diet. These data suggest that activation of the JAK/STAT pathway is critical for the development of ANG II-induced hypertension by mediating its effects on renal sodium excretory capability, but the physiological control of blood pressure by ANG II with a low-salt diet does not require JAK2 activation.

Relationships between Plasma Renin Activity and Urinary and Plasma Catecholamines

1974 ◽  
Vol 48 (s2) ◽  
pp. 287s-290s ◽  
Author(s):  
U. Werner ◽  
H. Günnewig ◽  
K. D. Bock
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Significant Positive Correlation ◽  
Plasma Renin ◽  
Primary Hypertension ◽  
Renin Activity ◽  
Positive Correlation ◽  
Noradrenaline Concentration

1. The relations between the changes in plasma renin activity (PRA) and urinary catecholamine excretion (UCA) or plasma noradrenaline concentration have been investigated (a) in patients with benign primary hypertension, with renovascular hypertension and with idiopathic asympatheticotonic hypotension (ASH), and (b) during orthostasis and after administration of frusemide, of the β-blocking agent tenormin, of clonidine and of dihydralazine. 2. In primary hypertension noradrenaline and mean arterial pressure (Pm) showed a close positive correlation. 3. The mean values of both PRA and UCA were higher in renovascular hypertension than in primary hypertension and extremely low in ASH. The overlap of individual values between the patient groups was markedly reduced by using the quotient PRA/UCA. There was a statistically significant positive correlation between PRA and UCA in primary hypertension and in renovascular hypertension, with a different slope of the regression lines. 4. The increase of PRA and of noradrenaline during orthostasis was closely correlated. Frusemide and β-receptor blockade changed the slope of the regression line by additional stimulation or inhibition respectively of PRA. 5. Clonidine decreased, and dihydralazine increased both PRA and noradrenaline concentration. These changes again showed a significant positive correlation. The fall of mean arterial pressure produced by clonidine was correlated with the decrease of PRA and of noradrenaline concentration.

scholarly journals Deoxycorticosterone Suppresses the Effects of Losartan in Nitric Oxide—Deficient Hypertensive Rats

2000 ◽  
Vol 11 (11) ◽  
pp. 1995-2000
Author(s):  
MARIA C. DE GRACIA ◽  
ANTONIO OSUNA ◽  
FRANCISCO O'VALLE ◽  
RAIMUNDO G. DEL MORAL ◽  
ROSEMARY WANGENSTEEN ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Ang Ii ◽  
Hypertensive Rats

Abstract. Chronic inhibition of the renin angiotensin system prevents increased BP and renal injury in NG-nitro-L-arginine methyl ester (L-NAME) hypertension. However, a relationship between plasma renin activity and the protective effect of chronic angiotensin II (Ang II) blockade has not been established. With this background, this study was undertaken to evaluate how the chronic administration of deoxycortisone acetate (DOCA) modifies the effects of losartan on BP, renal injury, and other variables in L-NAME hypertensive rats. The following groups were used: Control, DOCA, L-NAME, L-NAME + losartan, L-NAME + DOCA, and L-NAME + DOCA + losartan. Tail systolic BP was measured twice a week. After 4-wk evolution, mean arterial pressure and metabolic, morphologic, and renal variables were measured. The final mean arterial pressure values were 116 ± 6 mmHg for control, 107 ± 2 mmHg for DOCA, 151 ± 5 mmHg for L-NAME, 123 ± 2 mmHg for L-NAME + losartan, 170 ± 3 mmHg for L-NAME + DOCA, and 171 ± 5.5 mmHg for L-NAME + DOCA + losartan. Losartan prevented microalbuminuria, hyaline arteriopathy, and glomerulosclerosis of L-NAME hypertension but was ineffective in L-NAME + DOCA—treated rats. Plasma protein was significantly reduced in the L-NAME + DOCA group when compared with control and L-NAME groups, whereas no significant differences were observed in the other groups. Plasma renin activity was suppressed in the DOCA (0.55 ± 0.2) and L-NAME + DOCA (0.60 ± 10.2) groups but unsuppressed in the L-NAME + DOCA + losartan group (5.8 ± 1). The conclusion is that DOCA blocks the preventive effect of losartan on the increased BP and renal injury of L-NAME hypertension, which suggests that DOCA transforms L-NAME hypertension into an Ang II—independent model of hypertension. These data also suggest that losartan prevents L-NAME hypertension by blocking the activity of systemic Ang II.

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