Electrical stimulation of paraventricular nucleus increases plasma renin activity

1988 ◽  
Vol 254 (2) ◽  
pp. R325-R330 ◽  
Author(s):  
J. P. Porter

Studies employing direct electrical stimulation of the renal nerves have shown that, depending on the frequency used, selective effects on renal function can be evoked. With low frequencies, an increase in renin secretion can be elicited without affecting glomerular filtration rate, sodium excretion, or renal blood flow. In the present investigation the possibility was addressed that the central nervous system (CNS) is also organized to evoke selective changes in renal function. The paraventricular nucleus (PVN) of the hypothalamus was electrically stimulated in conscious rats with 150 microA and frequencies of 2.5, 5, 10, and 15 Hz. Blood samples for determination of plasma renin activity (PRA) were collected before and at the end of each 5-min stimulation period. The lower frequencies had no effect on PRA, but stimulation with 10 and 15 Hz produced a significant increase. This effect on PRA was not accompanied by changes in arterial pressure or renal blood flow. In a separate group of animals, stimulation of the PVN with 15 Hz produced a marked decrease in urine volume, but sodium excretion did not change. These data raise the possibility that the CNS is organized to evoke selective increases in sympathetic outflow to the kidney and to produce separate changes in renal functions.

1982 ◽  
Vol 5 (2) ◽  
pp. 57-67
Author(s):  
H.-H. Neumayer ◽  
K. Wagner ◽  
G. Schuhze ◽  
P. Laubner ◽  
M.K. Maiga ◽  
...  

1986 ◽  
Vol 71 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Mr J. K. Evans ◽  
P. F. Naish ◽  
G. M. Aber

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.


1995 ◽  
Vol 80 (Supplement) ◽  
pp. SCA26
Author(s):  
L. D. Testa ◽  
R. L. Royster ◽  
D. D. Deal ◽  
M. Gowda ◽  
J. F. Butterworth

1988 ◽  
Vol 254 (3) ◽  
pp. H509-H516 ◽  
Author(s):  
M. Burnier ◽  
B. Waeber ◽  
J. F. Aubert ◽  
J. Nussberger ◽  
H. R. Brunner

A nonhypotensive dose of endotoxin was administered to normal conscious rats to evaluate the vascular and humoral effects of endotoxemia per se. Mean blood pressure and heart rate remained stable during the 45 min infusion of Escherichia coli endotoxin (0.01 mg/min). However, a marked increase in plasma renin activity (4.2 +/- 0.48 vs. 30.2 +/- 6 ng.ml-1.h-1, mean +/- SE, P less than 0.01), plasma epinephrine (0.112 +/- 0.04 vs. 1.71 +/- 0.5 ng/ml, P less than 0.01), and plasma norepinephrine (0.269 +/- 0.028 vs. 1.3 +/- 0.2 ng/ml, P less than 0.001) was observed during infusion in endotoxin-treated rats when compared with the vehicle-treated animals. In addition, the blood pressure response to exogenous norepinephrine was significantly reduced during nonhypotensive endotoxemia. Significant changes in regional blood flow distribution, as assessed by radiolabeled microspheres, were observed in endotoxemic rats; in particular a decrease in renal blood flow (7.39 +/- 0.43 vs. 5.97 +/- 0.4 ml.min-1.g-1, P less than 0.05) and an increase in coronary blood flow (5.01 +/- 0.38 vs. 6.44 +/- 0.33 ml.min-1.g-1, P less than 0.01) were found. The role of prostaglandins in the vascular and humoral alterations induced by nonhypotensive endotoxemia was also examined. Pretreatment with indomethacin (5 mg) prevented the increase in plasma renin activity as well as plasma catecholamine levels. On the contrary, the decreased vascular reactivity and the reduction in renal blood flow observed during endotoxemia were not affected by prostaglandin synthesis inhibition. Thus significant vascular and humoral changes have been found during endotoxemia even in absence of hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)


1982 ◽  
Vol 63 (4) ◽  
pp. 355-360 ◽  
Author(s):  
P. C. Wong ◽  
B. G. Zimmerman

1. The blood pressure and renal blood flow response to captopril (0·2 mg/kg, intravenously) was studied in low salt, normal, and high salt fed conscious dogs, and in a group of DOCA-salt treated dogs. 2. Mean arterial blood pressure was decreased and renal blood flow increased most in the low salt group, but significant changes were also obtained in the normal group. The high salt and DOCA-salt groups were only marginally affected by captopril. 3. When the data from all four groups of dogs were subjected to regression analysis, there was a significant relationship (r = 0·68) between the prevailing plasma renin activity and the increase in renal blood flow caused by captopril. 4. The results suggest that renal vasodilatation resulting from converting enzyme inhibition is mainly due to a decrease in the level of circulating angiotensin II, and that even in the normal conscious dog the prevailing plasma renin activity can affect blood pressure and renal blood flow.


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