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

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.

1983 ◽  
Vol 244 (6) ◽  
pp. R823-R831
Author(s):  
W. J. Ray ◽  
M. L. Zatzman

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.


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

1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.


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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