Acute Effect of Physiological Concentrations of Vasopressin on Rat Renal Function (original) (raw)
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Dose-response effects of pressor doses of arginine vasopressin on renal haemodynamics in the rat
The Journal of Physiology, 1988
1. Dose-response effects of arginine vasopressin on renal haemodynamics were studied in conscious and in pentobarbitone-anaesthetized rats infused with 77 mm-NaCl at 5-2 and 2X6 ml h-1 respectively. 2. Vasopressin at 0X8 pmol h-1 (100 g body weight)-' did not have a significant effect on arterial blood pressure in conscious or anaesthetized rats. Increasing the dose to 2-5 pmol h-1 (100 g body weight)-' induced a pressor effect in conscious rats but not in anaesthetized rats. A pressor response was observed in the latter at a dose of 10 pmol h-1 (100 g body weight)-'. 3. Pressor doses of vasopressin of 100 pmol h-1 (100 g body weight)-' and less did not significantly alter the clearance of p-aminohippurate (PAH) in either conscious or anaesthetized rats. A dose of 1000 pmol h-1 (100 g body weight)-' significantly decreased PAH clearance in both conscious and anaesthetized animals. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin in both conscious and anaesthetized rats. Moderately pressor doses decreased inulin clearance in conscious animals only. The highest dose administered (1000 pmol h-1 (100 g body weight)-') decreased inulin clearance in both conscious and anaesthetized rats. 5. Pressor doses of vasopressin had a biphasic effect on the filtration fraction in conscious rats. The filtration fraction decreased with doses of vasopressin at the lower end of the pressor range but increased with the highest dose of 1000 pmol h-1 (100 g body weight)-'. In contrast the filtration fraction did not change significantly with moderate pressor doses in anaesthetized rats but was increased by doses of 100 and 1000 pmol h-1 (100 g body weight)-'. 6. It is concluded that pressor doses of vasopressin lower than 100 pmol h-' (100 g body weight)-' do not decrease renal plasma flow rate in conscious or pentobarbitone-anaesthetized rats. The results suggest that the inconsistent effects of vasopressin on renal blood flow reported in the literature are due, at least in part, to the wide range of doses used.
Renal haemodynamic actions of pressor doses of lysine vasopressin in the rat
The Journal of Physiology, 1987
1. Dose-response effects of lysine vasopressin on renal haemodynamics were studied in conscious rats infused with 2-5 % (w/v) dextrose solution at 5'8 ml/h. 2. Lysine vasopressin was maximally antidiuretic in the absence of a significant pressor effect at a dose of 2-5 pmol h-' 100 g body weight-'. Doses of vasopressin greater than this induced a dose-dependent increase in arterial blood pressure. 3. The clearance of p-aminohippurate (PAH) was not significantly changed by vasopressin, even at pressor doses. Rats pre-treated with indomethacin to inhibit prostaglandin synthesis showed a decrease in PAH clearance during the infusion of vasopressin at a dose of 30 pmol h-' 100 g body weight-', and this suggests that the renal vasoconstrictor actions of vasopressin are attenuated by dilator prostaglandins. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin but was decreased in a dose-dependent manner by pressor doses. A maximal effect was induced by a dose of 30 pmol h-' 100 g body weight-' which decreased inulin clearance from 3-23+0-76 (mean+s.E. of mean) to 1-60+0-37 ml/min (P < 0-02). A change in inulin clearance (from 3-42 +0-46 to 2-17 +0-33 ml/min, P < 0-01) was also observed in rats pre-treated with indomethacin and infused with vasopressin at the same dose. The magnitude of the change was not significantly different from that observed in rats which were not treated with indomethacin. 5. Control rats infused with dextrose showed a slight but significant increase in sodium excretion during the course of the experiment. A similar natriuresis was observed in rats infused with non-pressor doses of vasopressin but was considerably enhanced in rats infused with pressor doses of the peptide. The antidiuresis induced by vasopressin remained maximal in rats infused with pressor doses. 6. Potassium and osmolal outputs were unchanged by non-pressor doses of vasopressin but significantly increased during administration of pressor doses. 7. It is concluded that pressor doses of lysine vasopressin do not alter total renal perfusion in conscious rats when the prostaglandin system is intact. Glomerular filtration is, however, decreased in a dose-dependent manner by these amounts but the mechanism is unclear.
Autonomic Neuroscience-basic & Clinical, 2004
In this study we investigated the influence of d(CH 2 ) 5 -Tyr(Me)-[Arg 8 ]vasopressin (AAVP) and [adamanteanacetyl 1 ,0-ET-D-Tyr 2 ,Val 4 ,aminobutyryl 6 ,Arg 8,9 ]-[Arg 8 ]vasopressin (ATAVP), which are antagonists of vasopressin V 1 and V 2 receptors, and the effects of losartan, a selective angiotensin AT 1 receptor antagonist, and CGP42112A, a selective AT 2 receptor antagonist, injected into the lateral septal area (LSA) on thirst and hypertension induced by [Arg 8 ]vasopressin (AVP). AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT 1 and AT 2 ligands administered into the LSA elicited a concentrationdependent decrease in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of AAVP from 18 F 1 to 6 F 1 mm Hg. Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 F 0.8 mm Hg. ATAVP and CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT 1 receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple AVP and angiotensin II receptor subtypes. The pressor response of AVP was reduced by losartan and by AAVP. CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of V 1 receptors and that the inhibitory effect requires V 2 receptors. The involvement of AT 1 and AT 2 receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance. D
Vasopressin influences renal function via a spinal action
Brain Research, 1985
Intrathecal injections of arginine vasopressin (AVP) (3 pmol) into the lower thoracic region in rats produced consistent, dose-dependent antidiuretic responses accompanied by elevated urine osmolality. That these responses are not due to leakage of the peptide to the periphery is suggested by (a) the lack of response to the analogue, DDAVP, and (b) the lack of antidiuretic response to intrathecal AVP in denervated kidneys.
Osmoreceptors, vasopressin, and control of renal water excretion
Physiological Reviews, 1980
October 1980 OSMORECEPTORS AND RENAL WATER EXCRETION 963 found that the kidney secreted large amounts of dilute urine unless postpituitary extract was added to-or the head of a dog included in-the perfusion circuit. The significance of these observations was greatly increased by the work of Klisiecki et al. (254,255). Using conscious, chronically prepared dogs they made a series of pertinent observations on water absorption and excretion and concluded their work with a statement that has withstood the test of time: The secretion of water, over and above that required for the solutes of the urine, is conditioned by and dependent upon a fall in the concentration in blood and kidney of the antidiuretic principle of the pituitary body. The secretion of the antidiuretic principle is itself controlled, through the intermediation of the nervous system, by the concentration of water in blood and tissues.
Contribution of vasopressin to progression of chronic renal failure: Study in Brattleboro rats
Life Sciences, 1999
We have previously shown that a chronic reduction in plasma vasopressin level slowed the progression of chronic renal failure (CRF) in Sprague Dawley rats. The aim of the present study was to determine the respective contribution of pressor (Vl) and antidiuretic (V2) effects of vasopressin on progression. Male homozygous Brattleboro rats with hereditary central diabetes insipidus were submitted to 516 nephrectomy. They were divided into three groups, two of which received chronic i.p. infusion of AVP (Vl + V2 effects) or dDAVP (V2 effects). The third group served as control (CONT). The doses of AVP and dDAVP were chosen so as to produce urine osmolality similar to that observed in 5/6 Nx Sprague Dawley rats. All rats ate the same amount of food and drank water ad libitum. Renal function was studied for 13 weeks. All three groups showed a marked hypertension. Rats infused with dDAVP, but not those infused with AVP, had a higher creatininemia, anemia and urinary protein excretion than CONT rats. In the dDAVP but not the AVP group, fractional excretion of urea was markedly decreased and plasma urea concentration rose much more than that of creatinine. These results show that V2 but not Vl effects play a major role in the deleterious influence of vasopressin on progression, at least in Brattleboro rats. The more severe progression seen in dDAVP rats could indirectly result from the V2mediated effects on the collecting duct resulting in a decreased efficiency of urea excretion, an increased intrarenal urea recycling, and a rise in plasma urea concentration. Both the toxic effects of urea and the recently demonstrated VZmediated increase in glomerular hemodynamics might be involved in the deleterious influence of V2 ago&m.
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2000
Saline was infused intravenously for 90 min to normal, sodium-replete conscious dogs at three different rates (6, 20, and 30 µmol • kg Ϫ1 • min Ϫ1) as hypertonic solutions (HyperLoad-6, HyperLoad-20, and HyperLoad-30, respectively) or as isotonic solutions (IsoLoad-6, IsoLoad-20, and IsoLoad-30, respectively). Mean arterial blood pressure did not change with any infusion of 6 or 20 µmol • kg Ϫ1 • min Ϫ1. During HyperLoad-6, plasma vasopressin increased by 30%, although the increase in plasma osmolality (1.0 mosmol/kg) was insignificant. During HyperLoad-20, plasma ANG II decreased from 14 Ϯ 2 to 7 Ϯ 2 pg/ml and sodium excretion increased markedly (2.3 Ϯ 0.8 to 19 Ϯ 8 µmol/min), whereas glomerular filtration rate (GFR) remained constant. Iso-Load-20 decreased plasma ANG II similarly (13 Ϯ 3 to 7 Ϯ 1 pg/ml) concomitant with an increase in GFR and a smaller increase in sodium excretion (1.9 Ϯ 1.0 to 11 Ϯ 6 µmol/min). HyperLoad-30 and IsoLoad-30 increased mean arterial blood pressure by 6-7 mmHg and decreased plasma ANG II to ϳ6 pg/ml, whereas sodium excretion increased to ϳ60 µmol/min. The data demonstrate that, during slow sodium loading, the rate of excretion of sodium may increase 10-fold without changes in mean arterial blood pressure and GFR and suggest that the increase may be mediated by a decrease in plasma ANG II. Furthermore, the vasopressin system may respond to changes in plasma osmolality undetectable by conventional osmometry. angiotensin II; volume expansion; vasopressin; blood pressure; natriuresis.