A new specific RIA for alpha-human atrial natriuretic hormone (alpha hANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma alpha hANP and AVP levels were 51.3 +/- 16.0 (+/- SE) and 3.1 +/- 0.6 pg/ml, respectively, in the basal state. Plasma alpha hANP rose to 77.8 +/- 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 +/- 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 +/- 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P less than 0.01-0.05). On the other hand, plasma AVP fell to 1.8 +/- 0.1 pg/ml after the water load, rose to 4.1 +/- 0.6 after hypertonic saline, and rose further to 5.8 +/- 0.8 pg/ml after furosemide (P less than 0.01-0.05). Water and hypertonic saline loading decreased PRA, but plasma aldosterone concentrations did not change; subsequent furosemide administration increased both (P less than 0.01-0.05). Arterial pressure and heart rate did not change significantly. Increases in urinary Na excretion and osmolar clearances were associated with a rise in plasma alpha hANP after water loading and hypertonic saline infusion (P less than 0.01-0.05), but changes in urine flow were mainly associated with alterations in AVP release. associated with alterations in AVP release.
Rats with kidney isografts have a limited capacity to concentrate urine and, at the same time, fail to increase rBSC1 and AQP2 transcripts. This suggests that there is a prolonged damage of renal tubules by ischemia or denervation of the donor kidney, both of which are inevitable in the transplantation procedure.
In order to investigate the role of central noradrenergic neurons in the control of vasopressin (ADH) release and cardiovascular regulation, norepinephrine (1.4 microgram/kg), clonidine (0.1 microgram/kg), and isoproterenol (1.4 microgram/kg were infused into the lateral cerebral ventricle of the anesthetized dog. The drugs were given over a 20-min period, dissolved in 0.9% saline at a volume rate of 10 microliter/min. Both norepinephrine and clonidine markedly reduced ADH release and lowered arterial blood pressure and heart rate. Isoproterenol had no effect on ADH release and produced a slight reduction in arterial pressure and a large increase in heart rate. Pretreatment with phenoxybenzamine (100 microgram/kg, iv) completely blocked the effects of norepinephrine on blood pressure and heart rate but only partially (about 50%) inhibited the norepinephrine effect on ADH release. Intravenous isoproterenol lowered blood pressure and increased ADH release and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality or plasma sodium and potassium concentrations. It is concluded that, in the anesthetized dog, intraventricular norepinephrine and clonidine decreased ADH release, blood pressure, and heart rate by stimulating alpha-adrenoreceptors. The increased release of ADH after peripheral administration of isoproterenol was presumably due to the reduction in blood pressure and decreased baroreceptor inhibition of ADH release.
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