Circulating Dopamine: Its Effect on the Plasma Concentrations of Catecholamines, Renin, Angiotensin, Aldosterone and Vasopressin in the Conscious Dog

1981 ◽  
Vol 61 (4) ◽  
pp. 417-422 ◽  
Author(s):  
S. G. Ball ◽  
M. Tree ◽  
J. J. Morton ◽  
G. C. Inglis ◽  
R. Fraser
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Control Period ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Dopamine Infusion ◽  
Renin Angiotensin ◽  
Arterial Blood

1. Six male beagle dogs with carotid loops were infused with sodium chloride solution (150 mmol/l: saline) during control observations followed by dopamine infusion at various rates. Arterial blood samples were drawn during the control period and at the end of each period of dopamine infusion for the measurement of plasma dopamine, noradrenaline, adrenaline, renin, angiotensin II, aldosterone, vasopressin, electrolytes and packed cell volume. Blood pressure and pulse were recorded throughout. 2. The rate of infusion and plasma dopamine levels were closely correlated (r = 0.99, P < 0.001). Plasma dopamine levels two to 20 times basal values produced no significant change in any of the other variables measured; levels 200 times basal values caused a significant increase (P < 0.05) in plasma renin concentration; levels 2000 times basal values were associated with significant increases (P < 0.05) in plasma renin and angiotensin II, packed cell volume and blood pressure, without significant changes in other measurements. 3. Circulating dopamine is unlikely to be important in the control of sodium and water metabolism.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Renin-angiotensin-aldosterone system of the normothermic marmot

1977 ◽  
Vol 233 (1) ◽  
pp. R37-R43
Author(s):  
P. R. Kastner ◽  
M. L. Zatzman ◽  
F. E. South ◽  
J. A. Johnson
Keyword(s):  
Blood Pressure ◽  
Mammalian Species ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Salt Loading ◽  
Renin Angiotensin ◽  
Adrenal Steroid ◽  
Adrenal Secretion ◽  
Na Depletion ◽  
Secretion Rates

Adrenal steroid secretion rates and the renin-angiotensin-aldosterone (RAA) system were studied in the normothermic marmot. Adrenal secretion by the anesthetized, laparotomized marmot was (mean +/- SEM); aldosterone 1.2 +/- 0.3 ng/min, deoxycorticosterone 16.7 +/- 11.5 ng/min, corticosterone 15.2 +/- 7.8 ng/min, and cortisol 554 +/- 108 ng/min. Four forcings were investigated that affect feedback control at different sites: adrenocorticotropic hormone (ACTH) and angiotensin II (AII) infusion, sodium (Na) depletion, and Na loading. Plasma aldosterone, cortisol, Na, and potassium (K) concentrations as well as plasma renin activity (PRA) hematocrit (Hct), and in some studies, blood pressure were measured. ACTH infusion increased the plasma concentrations of aldosterone and cortisol. AII infusion increased aldosterone concentration, blood pressure, and Hct. Na depletion increased aldosterone, Hct, and PRA; plasma Na and K were decreased. Aldosterone concentration, Hct, and PRA decreased after salt loading. Normothermic, salt-depleted marmots demonstrated a pronounced fall in blood pressure following infusion of the AII analog, 1-sarcosine-8-alanine AII. The average plasma values for aldosterone, PRA, and cortisol found in 44 control animals were: aldosterone 3.8 +/- 0.3 ng/100 ml, PRA 1.9 +/- 0.2 ng AI-ml-1-h-1, and cortisol 54 +/- 4 ng/ml. It was concluded that normothermic marmots have a RAA system comparable to other mammalian species.

Effects of hyperinsulinaemia on the cardiovascular responses to graded hypovolaemia in normal and diabetic subjects

1988 ◽  
Vol 75 (1) ◽  
pp. 85-92 ◽  
Author(s):  
A. R. Scott ◽  
T. Bennett ◽  
I. A. MacDonald
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Normal Male ◽  
Euglycaemic Clamp ◽  
Arterial Blood ◽  
Hyperinsulinaemic Euglycaemic Clamp

1. Two experiments were carried out. The first with five normal male subjects was placebo controlled and single blind, each subject being studied on two occasions. Lower body subatmospheric pressure (LBSP) was used to assess the cardiovascular effects of graded hypovolaemia before and during either a hyperinsulinaemic, euglycaemic clamp or a placebo clamp using 0.9% (w/v) NaCl only. 2. During hyperinsulinaemia, resting systolic blood pressure rose and was accompanied by forearm vasodilatation. Forearm blood flow (FABF) and heart rate (HR) were higher at each level of LBSP during than before hyperinsulinaemia. In addition, hyperinsulinaemia was accompanied by a small increase in noradrenaline, but packed cell volume did not change. 3. In the second experiment, the effects of a hyperinsulinaemic euglycaemic clamp on the cardiovascular responses to LBSP were assessed in seven diabetic subjects with peripheral and autonomic neuropathy. 4. In contrast to the normal subjects, there was a slight fall in systolic blood pressure during the clamp but no effect was noted on HR or FABF. Mean arterial blood pressure was lower at each level of LBSP during hyperinsulinaemia compared with the pre-elamp period. Packed cell volume fell during the clamp and plasma noradrenaline rose. In one of the diabetic subjects, a precipitous fall in blood pressure occurred during hyperinsulinaemia when LBSP of 10 mmHg (1.3 kPa) was applied, this manoeuvre having been well tolerated before the clamp. 5. The mode of action of hyperinsulinaemia is not clear, but there was, however, no evidence that a fall in plasma volume had occurred.

Renin-angiotensin system in hypophysectomized rats. I. Control of blood pressure

1984 ◽  
Vol 246 (1) ◽  
pp. E84-E88
Author(s):  
C. D. Simon ◽  
T. W. Honeyman ◽  
J. C. Fray
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Hormone Administration ◽  
Hypophysectomized Rats

The mechanisms whereby the pituitary gland maintains arterial pressure were investigated in rats. The arterial pressure in hypophysectomized rats was 30 mmHg below normal. Saralasin or captopril caused a further fall of 25 and 30 mmHg, respectively, suggesting that the renin-angiotensin system plays a role in blood pressure maintenance in hypophysectomized rats. Growth hormone administration to hypophysectomized rats increased the arterial pressure, but pretreatment with captopril prevented the effect. Plasma renin activity and basal renin secretion (in vitro) was normal in hypophysectomized rats despite a twofold greater renal renin content. Secretory responsiveness to isoproterenol and calcium omission was lower in hypophysectomized rats. It is concluded that the renin-angiotensin system plays a role in maintaining arterial blood pressure in hypophysectomized rats although the responsiveness of the system may be decreased.

Plasma renin activity, angiotensin II, and aldosterone during intense heat stress

1976 ◽  
Vol 41 (3) ◽  
pp. 323-327 ◽  
Author(s):  
K. J. Kosunen ◽  
A. J. Pakarinen ◽  
K. Kuoppasalmi ◽  
H. Adlercreutz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Blood ◽  
Main Components ◽  
Intense Heat

Plasma renin activity (PRA), angiotensin II, and aldosterone levels, arterial blood pressure, and heart rate of six male students were investigated during and after heat stress in a sauna bath. Increased PRA, angiotensin II, and aldosterone levels were found both during and after sauna. The greatest mean increases in PRA (94.9 +/- 10.4% SE, P less than 0.005) and angiotensin II (196 +/- 54.7% SE, P less than 0.02) were observed at the end of the heat stress (at 20 min), and that in plasma aldosterone (505 +/- 209% SE, P less than 0.02) 30 min after the sauna. The heart rate roughly doubled during the heat stress and there was a transient increase followed by a decrease in systolic blood pressure and a decrease in diastolic blood pressure. This study demonstrates that intense heat stress can cause remarkable changes in the three main components of the renin-angiotensin-aldosterone system.

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids

1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na+−K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 ± 3.9 to 146.4 ± 2.7 mmHg, P < 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 ± 1.8 to 124.1 ± 3.6 mmHg, P < 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 ± 6.9 and 159.8 ± 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 ± 1.2 to 116.9 ± 1.7 mmol/l of cells, P < 0.001), in erythrocyte Na+ concentration (from 14.3 ± 0.8 to 13.0 ± 0.6 mmol/l of cells, P < 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 ± 0.3 to 16.0 ± 0.4 mmol h−1 (1 of cells)−1, P < 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 ± 0.2 to 10.4 ± 0.2 mmol h−1 (1 of cells)−1, P < 0.01). No change in blood pressure, erythrocyte cation concentration or Na+−K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone. 4. The hypertensive influence of oestradiol in normotensive rats was unaccompanied by any changes in erythrocyte K+ concentration, erythrocyte Na+ concentration and total, ouabain-sensitive and ouabain-resistant Na+−K+ flux. 5. The divergent changes in blood pressure noted in the two strains occurred despite comparable changes in plasma renin activity after oestradiol, with significant increases in plasma renin activity in normotensive rats (from 16.4 ± 4.2 to 28.4 ± 6.6 ng of angiotensin I h−1 ml−1, P < 0.05) and in spontaneously hypertensive rats (from 28.3 ± 2.7 to 39.5 ± 5.7 ng of angiotensin I h−1 ml−1, P < 0.01). The plasma renin activity in spontaneously hypertensive rats receiving oestradiol or indomethacin and oestradiol were similar with values of 39.5 ± 5.7 and 40.6 ± 5.7 ng of angiotensin I h−1 ml−1, respectively, but were significantly higher than that seen in control animals (28.3 ± 2.7 ng of angiotensin I h−1 ml−1, P < 0.01). Similarly, indomethacin alone induced a significant increase in plasma renin activity in spontaneously hypertensive rats to 35.8 ± 7.6 ng of angiotensin I h−1 ml−1 (P < 0.05). 6. The contrasting effects of oestradiol on blood pressure in the two rat strains occurred without any change in packed cell volume. Likewise, the changes in blood pressure in spontaneously hypertensive rats with either oestradiol alone or in combination with indomethacin occurred without any change in packed cell volume, although indomethacin alone resulted in a significant reduction in packed cell volume (from 30.9 ± 1.6 to 26.8 ± 2.0, P < 0.01). 7. The results suggest that the hypotensive action of oestradiol in spontaneously hypertensive rats might be mediated through its influence on erythrocyte cation concentration and/or the modulation of Na+−K+ flux either directly or via the action of prostanoids.

Exaggerated blood pressure response to angiotensin II in patients with Cushing's syndrome due to adrenocortical adenoma

1994 ◽  
Vol 131 (6) ◽  
pp. 582-588 ◽  
Author(s):  
Gen Yasuda ◽  
Hiroshi Shionoiri ◽  
Satoshi Umemura ◽  
Izumi Takasaki ◽  
Masao Ishii
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cushing’S Syndrome ◽  
Blood Pressure Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Cushing's Syndrome ◽  
Adrenocortical Adenoma ◽  
Angiotensin System ◽  
Renin Angiotensin

Yasuda G, Shionoiri H, Umemura S, Takasaki I, Ishii M. Exaggerated blood pressure response to angiotensin II in patients with Cushing's syndrome due to adrenocortical adenoma. Eur J Endocrinol 1994:131:582–8 ISSN 0804–4643 We studied the roles played by the renin-angiotensin system in inducing hypertension in nine patients with Cushing's syndrome (CS) resulting from adrenocortical adenoma, and compared them with those in patients with primary aldosteronism (PA), renovascular hypertension (RVH) and essential hypertension (EH). In the CS group, each parameter, including serum potassium, plasma renin activity, plasma aldosterone, deoxycorticosterone and corticosterone concentrations, is within the normal range. However, plasma renin activity in the CS group was lower than that in the RVH group but higher than that in the PA group, and plasma aldosterone concentration was lower than that in each RVH or PA group. These findings indicated that the CS group had a different type of hypertension from that in either RVH or PA, in which the renin angiotensin system or mineralocorticoids play an important role in hypertension. Meanwhile, captopril (50 mg) administration either with or without indomethacin pretreatment decreased the mean blood pressure in the CS group, although captopril failed to change it in the PA group or in normal subjects. Furthermore, the pressor response to exogenous angiotensin II in the CS group was higher than that in the RVH or EH group, but was not different from that in the PA group. Thus, the hypertension in patients with CS due to adrenocortical adenoma appears to be mediated through a change in the renin-angiotensin system in the form of exaggerated pressor responses to angiotensin II. G Yasuda, Second Department of Internal Medicine, Yokohama City University School of Medicine, 3-46 Urafune, Minami, Yokohama 232, Japan

Response of Blood Pressure and the Renin—Angiotensin—Aldosterone System to Chronic Ambulatory Peritoneal Dialysis in Hypertensive End-Stage Renal Failure

1982 ◽  
Vol 63 (s8) ◽  
pp. 207s-209s ◽  
Author(s):  
Ph. Glasson ◽  
H. Favre ◽  
M. B. Vallotton
Keyword(s):  
Blood Pressure ◽  
Peritoneal Dialysis ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
End Stage ◽  
Chronic Ambulatory Peritoneal Dialysis

1. Chronic ambulatory peritoneal dialysis allows good control of blood pressure in patients with hypertensive end-stage renal disease. The role of the renin-angiotensin-aldosterone system has therefore been studied in seven patients during the first 6 months of chronic ambulatory peritoneal dialysis treatment. 2. Steady increases in plasma renin activity and aldosterone were observed with a good correlation between these two variables. Plasma electrolytes, renin substrate and body weight did not change significantly. 3. Angiotensin II perfusion tests, performed at the end of the study, showed a relative vascular resistance to angiotensin II. 4. Stimulation of the renin-angiotensin-aldosterone system may be partially explained by this last observation or by removal of an unknown vasopressor substance responsible for the inhibition of the plasma renin activity.

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs

1983 ◽  
Vol 245 (4) ◽  
pp. H667-H673
Author(s):  
D. B. Averill ◽  
A. M. Scher ◽  
E. O. Feigl
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Ang Ii ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.

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