Factors that alter the plasma renin activity of the marmot

1983 ◽  
Vol 244 (6) ◽  
pp. R823-R831
Author(s):  
W. J. Ray ◽  
M. L. Zatzman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Low Doses ◽  
Control Data ◽  
Volume Load

The effects of low doses of norepinephrine (NE) and furosemide and a volume load (nonhibernators only) on plasma renin activity (PRA), mean arterial pressure (MAP), heart rate (HR), left renal (RBF) and right iliac (IBF) blood flow, cardiac index (CI), and total peripheral resistance (TPR) were determined in euthermic and hibernating marmots. In nonhibernating marmots NE produced an increase in CI and TPR and a decrease in RBF. In hibernators this dose of NE caused an increase in MAP, HR, and renal resistance, whereas it decreased PRA and did not alter iliac resistance. Furosemide infusions led to an increase in PRA in both groups and an increase in TPR in nonhibernators. The volume load in nonhibernators produced only a decrease in PRA. A comparison of control data from the two groups indicated that the renal and iliac beds contribute only a small portion to the increase in TPR that occurs during hibernation.

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.

Oestrogen-induced changes in renal haemodynamics in the rat: Influence of plasma and intrarenal renin

1986 ◽  
Vol 71 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Mr J. K. Evans ◽  
P. F. Naish ◽  
G. M. Aber
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renal Haemodynamics ◽  
Renin Activity ◽  
Female Rats

1. The effect of oestrone acetate (in total doses of 5 and 10 mg) on systemic and renal haemodynamics and the renin-angiotensin system has been studied in adult female rats. 2. The administration of 10 mg of oestrogen resulted in a significant fall in renal blood flow associated with significant rises in both renal vascular resistance and mean arterial pressure. No changes were noted in cardiac output or total peripheral resistance at either dose. 3. Whilst the higher dose of oestrogen induced a significant increase in plasma renin activity, no change was noted in animals receiving 5 mg of oestrogen. Both regimens caused significant reductions in plasma and intrarenal renin concentrations. 4. Although renal blood flow correlated with plasma renin activity in animals with a normal renal blood flow, no such correlation was noted in animals with oestrogen-induced reductions in renal blood flow. 5. The present study demonstrates that oestrogen-induced reductions in renal blood flow result from a rise in intrarenal vascular resistance which cannot be accounted for by simultaneous changes in either plasma renin activity or renal renin concentration.

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.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

PROSTAGLANDIN MEDIATED NATRIURESIS DURING GLUCAGON INFUSION IN DOGS

1977 ◽  
Vol 84 (2) ◽  
pp. 429-438 ◽  
Author(s):  
Uffe Bang Olsen
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renin Activity ◽  
Conscious Dogs ◽  
Natriuretic Effect

ABSTRACT Ten μg/min glucagon infused intravenously for 30 min in conscious dogs (weight 15–25 kg) is shown to increase renal prostaglandin activity and to produce a natriuretic effect, which is impaired by indomethacin pretreatment. Cardiac output, heart rate, renal blood flow and urine cAMP excretion are similarly increased in non-pre-treated and indomethacin pre-treated dogs. Glucagon infusion does not consistently change plasma renin activity in non-pre-treated dogs, while the renin secretion is almost totally blocked when glucagon is administered to dogs that are pre-treated with indomethacin. The results are consistent with the view that the natriuretic response to glucagon is largely dependent upon increased renal blood flow. An addition tubular prostaglandin mediated and possible anti-aldosterone effect is, however, also involved.

High-Renin Essential Hypertension: Adrenergic Cardiovascular Correlates

1976 ◽  
Vol 51 (s3) ◽  
pp. 181s-184s ◽  
Author(s):  
M. Esler ◽  
S. Julius ◽  
O. Randall ◽  
V. Dequattro ◽  
A. Zweifler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Elevated Plasma ◽  
Sympathetic Nervous

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute β-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total peripheral vascular resistance at rest and a greater fall in peripheral resistance with α-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance. 3. Blood pressure was normalized by ‘total’ autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.

Mechanism of the Haemodynamic Interaction between Atenolol, a Cardioselective β-Adrenoreceptor-Blocking Agent, and Chlorthalidone in Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 363s-365s
Author(s):  
M. Velasco ◽  
J. Guevara ◽  
J. Morillo ◽  
A. Ramírez ◽  
A. Urbina-Quintana ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Time Interval ◽  
Calf Blood Flow

1. The effect of the cardioselective β-adrenoreceptor antagonist atenolol on blood pressure, heart rate, systolic time interval, limb blood flow and limb vascular resistance was studied, both when the drug was used by itself, and also when combined with chlorthalidone. Plasma renin activity and plasma atenolol concentration were also measured. 2. After the administration of atenolol alone, there was a decrease in mean blood pressure from 131·8 ± sem 2·88 mmHg to 119·0 ± 4·05 mmHg (P &lt; 0·001), in heart rate from 76·4 ± 3·58 beats/min to 57·0 ± 2·55 beats/min (P &lt; 0·001), in calf blood flow from 9·23 ± 1·39 ml min−1100 g−1 to 5·05 ± 0·89 ml min−1 100 g−1 (P &lt; 0·001), and an increase in calf vascular resistance from 16·54 ± 1·90 (mmHg min−1100 g−1)/ml to 28·53 ± 3·40 (mmHg min−1 100 g−1)/ml) (P &lt; 0·005). Atenolol did not alter the pre-ejection period index significantly (P &gt; 0·1). In atenolol-treated patients, upon addition of chlorthalidone there was a further decrease in mean blood pressure from 119·0 ± 4·05 mmHg to 105·9 ± 4·12 mmHg (P &lt; 0·001). There was no further significant alteration in heart rate, pre-ejection period index, calf blood flow or calf vascular resistance. 3. Atenolol decreased plasma renin activity from 4·69 ± 0·87 to 2·85 ± 0·68 ng h−1 ml−1 (P &lt; 0·05), and the addition of chlorthalidone increased it from 2·85 ± 0·68 to 3·81 ± 0·98 ng h−1 ml−1 (P &lt; 0·05). 4. There was a 7·8 fold-interindividual variability in the relationship between plasma atenolol concentration and the dose of atenolol after a single oral dose of 100 mg of the drug.

Differential maturation of beta-adrenoceptor-mediated responses in the lamb fetus

1988 ◽  
Vol 255 (5) ◽  
pp. R794-R798 ◽  
Author(s):  
N. M. Rawashdeh ◽  
J. C. Rose ◽  
N. D. Ray
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renin Activity ◽  
Functional Maturity ◽  
Beta Adrenoceptor ◽  
Beta Receptor

To study the functional maturity of beta-receptor-mediated responses, seven chronically catheterized lamb fetuses, 93-107 days of gestation, and seven fetuses, 116-134 days of gestation, received intravenous randomly sequenced infusions of isoproterenol (ISO) 0.03, 0.06, and 0.125 micrograms.kg-1.min-1 for 10 min separated by 45-min intervals or two saline infusions followed by 0.125 micrograms.kg-1.min-1 ISO after treatment with 0.5 mg/kg propranolol (PRO). Each fetus received the two treatments 24-48 h apart. In immature fetuses, plasma renin activity (PRA) of 2.0 +/- 0.7 ng.ml-1.h-1 did not change with either protocol. In mature fetuses, PRA of 7.5 +/- 2.5 ng.ml-1.h-1 increased two- to three-fold after the infusion of the highest two doses of ISO (P less than 0.003). Propranolol blocked this response. No significant changes were observed after the infusions of the lowest dose of ISO or saline. Both groups showed significant heart rate increases with all doses of ISO. Propranolol injection decreased heart rate significantly and blocked responses to ISO. We conclude that although a cardiac beta-receptor-mediated response is present by 93 days of gestation in the lamb fetus, a renal beta-receptor-mediated response, renin secretion, is absent.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Sign in / Sign up

Export Citation Format

Share Document