Reflex Control of Renin Release in Essential Hypertension

1978 ◽  
Vol 54 (3) ◽  
pp. 217-222 ◽  
Author(s):  
G. Mancia ◽  
G. Leonetti ◽  
Laura Terzoli ◽  
A. Zanchetti
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Tissue Pressure ◽  
Reflex Control

1. The reflex control of renin release was studied in subjects with essential hypertension by comparing the effects of a variable-pressure neck chamber and head-up tilting. 2. Increase in carotid sinus transmural pressure (obtained by reducing tissue pressure outside the carotid sinus by 34 ± 3 mmHg) decreased mean arterial pressure by 16 ± 2 mmHg, but did not reduce significantly the renal venous—arterial difference in plasma renin activity. Likewise decrease in carotid sinus transmural pressure (obtained by increasing tissue pressure outside the carotid sinus by 39 ± 2 mmHg) increased mean arterial pressure by 14 ± 3 mmHg, but caused only a very slight increase in the renal venous—arterial difference in plasma renin activity. 3. Passive tilting reduced mean arterial pressure by 9 ± 1 mmHg. In this circumstance the renal venous—arterial difference in plasma renin activity increased significantly and markedly. 4. It is concluded that in essential hypertension the carotid sinus baroreceptors, though active in blood pressure control, do not exert a major influence on renin release. In these patients reflex increase of renin during tilting is apparently mediated through other receptors than those in the carotid sinuses.

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.

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.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

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.

Effect of vasopressin blockade on blood pressure during water deprivation in intact and baroreceptor-denervated conscious dogs

1988 ◽  
Vol 254 (4) ◽  
pp. E490-E495 ◽  
Author(s):  
L. C. Gregory ◽  
E. W. Quillen ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation ◽  
Marked Contrast

Previous studies have provided evidence that vasopressin plays an important role in blood pressure regulation during water deprivation. However, these investigations have been complicated by reflex compensatory increases in cardiac output and renin secretion. The aim of the present study was to investigate the effect of blockade of the vasoconstrictor action of vasopressin in conscious water-deprived dogs in which the low- and/or high-pressure baroreceptors were denervated to minimize reflex responses. Vasopressin blockade in sham-operated dogs (n = 7) did not change arterial pressure. Heart rate rose from 78 +/- 9 to 119 +/- 13 beats/min (P less than 0.01), and plasma renin activity increased from 10.9 +/- 2.1 to 21.6 +/- 4.6 ng.ml-1.3 h-1 (P less than 0.01). In carotid sinus-denervated dogs (n = 6), vasopressin blockade again failed to decrease arterial pressure. Heart rate increased from 105 +/- 10 to 132 +/- 10 beats/min (P less than 0.01), and plasma renin activity rose from 6.8 +/- 1.7 to 15.5 +/- 2.4 ng.ml-1.3 h-1 (P less than 0.01). The antagonist also failed to change blood pressure in cardiac-denervated dogs (n = 5). Heart rate increased from 111 +/- 9 to 119 +/- 1 beats/min (P less than 0.01), but plasma renin activity did not increase significantly. In marked contrast, vasopressin blockade in sinoaortic/cardiac-denervated dogs (n = 7) promptly decreased arterial pressure from 115 +/- 8 to 94 +/- 7 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Postural Changes of Plasma Renin Activity after Renal Transplantation

1974 ◽  
Vol 48 (s2) ◽  
pp. 283s-286s
Author(s):  
A. Salvetti ◽  
F. Arzilli ◽  
P. Sassano ◽  
P. Gazzetti ◽  
P. Rindi
Keyword(s):  
Renal Transplantation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Inverse Correlation ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Blocking Agent ◽  
Renin Activity ◽  
Postural Changes

1. Postural changes of plasma renin activity (PRA) before and after the administration of a beta-blocking agent (oxprenolol) were studied in nine patients with renal homotransplantation and in ten normal subjects. 2. In normal subjects PRA always increased during upright posture without any correlation with postural changes in mean arterial pressure. Oxprenolol reduced the postural increase of PRA. 3. A postural increase of PRA could be detected as early as 20–25 days after renal transplantation, and appeared with increasing frequency as time elapsed. 4. There was a significant inverse correlation (r−0.794,P <0.001) between the postural changes of PRA and those of mean arterial pressure. 5. These results suggest that in patients with renal homotransplantation the postural increase of PRA can only partly be due to circulating catecholamines or the sympathetic nervous system and may be explained by inverse changes in the mean arterial pressure.

Effects of hypoproteinemia on fluid volumes and arterial pressure

1983 ◽  
Vol 245 (2) ◽  
pp. H284-H293 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Protein Concentration

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.

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.

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