Effects of Angiotensin on Plasma Electrolyte Concentrations in Rabbits and in Man

1974 ◽  
Vol 46 (1) ◽  
pp. 19-36
Author(s):  
J. K. Healy ◽  
A. J. Elliott ◽  
L. C. Harrison

1. The effects of an intravenous infusion of angiotensin on plasma electrolytes were examined in normal, adrenalectomized and nephrectomized groups of rabbits and in normal man. Rabbits were given 1 μg kg−1 min−1 and human subjects 0.008–0.030 μg kg−1 min−1 of angiotensin. 2. In normal rabbits, angiotensin increased arterial and venous plasma K within 2 min by 0.8 and 0.4 mmol l−1 respectively, some hyperkalaemia persisting for 30–60 min. After 60 min arterial plasma Na decreased by 3.8 mmol l−1 and Cl by 2.4 mmol l−1. Arterial blood pH increased 0.04 units after 15 min, and arterial plasma Mg and Ca rose slightly after 2 min. Pressor response was 20–28 mmHg. 3. In adrenalectomized and nephrectomized rabbits, arterial plasma K rose within 2 min by 2.6 and 3.8 mmol l−1 respectively. Arterial plasma Na fell after 60 min in both groups, and also after 2 min in nephrectomized animals. Venous plasma K and Na showed similar although less marked changes. Changes in plasma Mg, Ca and blood pH were not significant. Pressor response in both groups exceeded that in normal rabbits. 4. In man, a sustained rise of 0.2–0.3 mmol 1-1 occurred in arterial plasma K during angiotensin infusion. Arterial blood pH rose 0.01 units after 15 min. Pressor response was 12–15 mmHg. 5. It was concluded that plasma electrolyte levels may change during angiotensin administration in rabbits and man, and that these changes may influence interpretation of physiological actions of angiotensin.

1990 ◽  
Vol 123 (3) ◽  
pp. 345-352 ◽  
Author(s):  
V. Papapdopoulos ◽  
P. Kamtchouing ◽  
N. Boujrad ◽  
C. Pisselet ◽  
C. Perreau ◽  
...  

Abstract. Intracellular cyclic AMP and testosterone productions by purified mature rat Leydig cells were stimulated by oLH (25 μg/l) 18- and 12-fold, respectively, after a 5-h incubation period. The replacement of the incubation medium by charcoal-treated testicular venous plasma (40%, v/v) from adult rams in the breeding season induced an inhibition of cyclic AMP and testosterone productions (82 and 66%, respectively, of oLH-stimulated values). Testicular arterial plasma is less effective than testicular venous plasma, even when it originates from non-breeding season rams; in that case, testicular venous and arterial plasma strongly inhibit testosterone productions (84 and 67%, respectively of oLH-stimulated values), which probably indicates that the inhibitory activity is higher in the non-breeding season. The addition of peripheral plasma leads to a testosterone production equal to 35 and 65% of the oLH-stimulated values, respectively, for ram blood collected in non-breeding and breeding seasons. The same concentration of ovine testicular lymph or rete testis fluid is without significant effect on cyclic AMP production; however, testosterone is slightly decreased by lymph but enhanced by rete testis fluid. Increasing amounts of venous or arterial testicular blood induce a dose-related decrease of the specific binding of labelled hCG in both rat and ram testicular membranes. This inhibiting factor is present in peripheral and testicular blood of either control or hypophysectomized or castrated rams, is a protein in nature, heat-sensitive, and has an apparent molecular weight higher than 10 000 daltons. These results suggest the existence of a control of LH-specific binding to its receptors and of Leydig cell cyclic AMP and testosterone outputs; these activities are not species-specific and are more concentrated in testicular venous than in arterial blood. The origin of this inhibiting factor remains to be determined, since it is not confined to the testis and not of pituitary origin.


Blood ◽  
1960 ◽  
Vol 16 (4) ◽  
pp. 1433-1438 ◽  
Author(s):  
W. O. CRUZ ◽  
J. R. MAGALHAES ◽  
L. MEIS

Abstract Dog arterial and venous plasma and lymph were fractionated by Cohn method 10 and the fractions tested for inhibitory activity when added to normal arterial blood in the dog hind leg preparation adapted for studies on hemostasis. Cohn fraction IV from arterial or venous plasma and from lymph was the only fraction, at low concentrations, able to inhibit the hemostatic ability of normal arterial plasma. Some facts suggest that alpha-lipoproteins are the plasma constituent of fraction IV with inhibitory effect on normal arterial blood. Biochemical changes in blood plasma seem more important or more directly connected with the mechanism of normal hemostasis control than the participation of blood cellular elements.


1985 ◽  
Vol 104 (1) ◽  
pp. 143-148 ◽  
Author(s):  
E. C. Osborn ◽  
P. L. Sugden ◽  
J. C. Mackenzie ◽  
D. M. Aitken ◽  
I. D. Chapman ◽  
...  

ABSTRACT Angiotensin II and I significantly raised potassium and lowered sodium and chloride ion concentrations in arterial plasma, with peak changes occurring in the first 2 min of a 6-min infusion period. The octapeptide increased the arterial K+ level in a dose-dependent manner, but the response showed tachyphylaxis when multiple infusions of 6-min duration were administered after a recovery interval of only 5 min. Raising the arterial blood pressure by 20–33 mmHg with adrenaline and noradrenaline failed to account for the increase in arterial plasma K+ concentration produced by the two peptides. These findings, in particular the rise in K+ concentration, are discussed in relation to possible mechanisms by which angiotensin II affects arteriolar tone. J. Endocr. (1985) 104, 143–148


1970 ◽  
Vol 38 (2) ◽  
pp. 157-174 ◽  
Author(s):  
K. F. Hosie ◽  
J. J. Brown ◽  
A. M. Harper ◽  
A. F. Lever ◽  
R. F. MacAdam ◽  
...  

1. In anaesthetized dogs the rate at which renin was released into the circulation of the right and left kidneys was estimated from renal blood flow, haematocrit, and the V-A renin concentration difference across the kidney. Renin was also measured in samples of renal lymph collected at the same time. 2. The effect on renin release of reducing blood flow in one kidney was studied. For all observations (control and experimental), renal venous plasma renin concentration (RVR) was directly related to arterial plasma renin concentration and to renin release; RVR was inversely related to renal plasma flow. 3. The concentration of renin in renal lymph was considerably higher than that in renal venous plasma taken at the same time. Arterial plasma renin concentration was directly related to the sum of the rates at which renin was released from the two kidneys. 4. Clamping the renal artery of one kidney for 1 hr led to a marked reduction of renal blood flow, to a marked increase in RVR and to a variable change in renin release. Removal of the clamp was followed by increased renin release and by reversal of a previously positive V-A renin difference in the control kidney. 5. On several other occasions negative V-A renin differences were observed. That is, more renin appeared to enter the kidney in arterial blood than left in the renal vein.


1987 ◽  
Vol 252 (1) ◽  
pp. R145-R152
Author(s):  
B. C. Wang ◽  
G. F. Ginter ◽  
K. L. Goetz

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.


2001 ◽  
Vol 100 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Eleanor M. SCOTT ◽  
John P. GREENWOOD ◽  
Stephen G. GILBEY ◽  
John B. STOKER ◽  
David A. S. G. MARY

A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean±S.E.M.) from 42±4 to 58±5 impulses/100 beats (P < 0.01) and from 36±4 to 51±5 bursts/100 beats (P < 0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.


1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.


1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.


1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.


1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.


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