Mechanisms for the diuresis of acute cold exposure: role for vasopressin?

1993 ◽  
Vol 264 (3) ◽  
pp. R524-R532 ◽  
Author(s):  
D. E. Allen ◽  
M. Gellai

The hypothesis that inhibition of vasopressin (VP) secretion initiates cold-induced diuresis was tested in six Brattleboro homozygous (diabetes insipidus, DI) rats exposed to 60 min at 5 degrees C. For 9-14 days before cold exposure (CE) the rats were treated with VP (750 pg.kg-1.min-1) subcutaneously via osmotic minipumps. Eight vehicle-treated Long-Evans (LE) rats characterized the response to acute exposure at 5 degrees C. Additional groups of six to eight LE and six DI rats were infused with VP (30-90 pg.kg-1.min-1 iv) on the day of CE. The DI rats receiving chronic VP replacement and untreated LE rats exhibited cold-induced diuresis, with peak increases in urine flow (V) of 63 +/- 12 (DIs) and 29 +/- 4 (LEs) microliters.min-1 x 100 g body wt-1. LE rats acutely infused with VP exhibited a diuresis at the two lower doses (peak V was 18 +/- 3 at the 30 and 18 +/- 4 microliters.min-1 x 100 g body wt-1 at the 60 pg.kg-1.min-1 dose), but the diuretic response was completely blunted at the uppermost dose of VP. Cold-induced diuresis was absent at the lowest VP dose in the acutely infused DI rats. A pressor response (30-36 mmHg) to CE was noted with all treatment groups, including those that did not exhibit a diuresis. No changes in glomerular filtration rate (GFR) with CE were observed. These data suggest that when plasma VP levels are controlled by prolonged infusion of VP in the DI rats, other mechanisms can operate to initiate cold-induced diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

1965 ◽  
Vol 208 (6) ◽  
pp. 1093-1099 ◽  
Author(s):  
John K. Healy ◽  
Carlos Barcena ◽  
J. M. Brian O'Connell ◽  
George E. Schreiner

The renal and pressor actions of angiotensin in relation to dose were studied in unanesthetized dogs. Low doses caused depression of urine flow, electrolyte excretion, glomerular filtration rate (GFR), and Cpah. With higher doses, the initial depression of urine flow, GFR, and Cpah was greater, but subsequently these functions rose toward control values. In fact, diuresis occurred, accompanied by natriuresis, chloruresis, and kaliuresis. The natriuresis occurred at a time when GFR was significantly depressed. In longer experiments at high doses it was found that the natriuresis declined after 50 min despite continued angiotensin infusion; however, potassium excretion gradually increased throughout. These results help clarify the confusing literature regarding the effects of angiotensin on renal function in dogs and also support the hypothesis that angiotensin can block tubular sodium reabsorption. The pressor response was found to be proportional to the logarithm of the dose of angiotensin. It was also inversely related to the control blood pressure of the dog.


1978 ◽  
Vol 235 (2) ◽  
pp. F151-F155 ◽  
Author(s):  
P. K. Pang ◽  
W. H. Sawyer

Although mesotocin (MT) has long been known to occur in the amphibian neurohypophysis, there have been few reports on its action among amphibians. In the present investigation, renal responses of intact bullfrogs (Rana catesbeiana) and perfused bullfrog kidneys to MT were studied. The blood pressure responses of this amphibian to MT were also analyzed. We found that MT is diuretic at low doses and that the response is dose related. At high doses the diuretic response decreases progressively and, at times, antidiuresis is observed. The changes in urine flow are proportional to the changes in glomerular filtration rate. In addition, there is a dose-related depressor effect. Data from perfused kidney studies suggest that MT may dilate the afferent glomerular vessels. The possible action of MT as a physiologically important diuretic agent is discussed.


1988 ◽  
Vol 255 (5) ◽  
pp. H1018-H1023 ◽  
Author(s):  
R. M. Thornton ◽  
J. M. Davidson ◽  
S. Oparil

This study sought to determine whether spontaneously hypertensive rats (SHR) on a high-NaCl diet have an enhanced pressor response to acute cold exposure and to define the peripheral mechanisms involved in the enhanced pressor response. SHR and normotensive Wistar-Kyoto (WKY) rats that had been on 1 and 8% NaCl diets for 3 wk were subjected to cold exposure. After a 30-min control period, animals were exposed to cold (6 +/- 2 degrees C) for 90 min. Mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured continuously. In a separate group of SHR on 1 and 8% NaCl diets, an arginine vasopressin (AVP) V1 receptor antagonist (10 micrograms/kg iv) was given before cold exposure, and MAP was measured throughout cold exposure. Plasma AVP was measured before and during cold exposure in a separate group of SHR. During cold exposure, there was a significant increase (P less than 0.05) in MAP (25 mmHg) in SHR on the 8% NaCl diet only. In contrast, HR and LSNA increased similarly during cold exposure in both SHR and WKY on the two diets. AVP was similar in both SHR groups (7.1 pg/ml for 1% vs. 6.1 pg/ml for 8%) before cold exposure, but during cold exposure it increased in the 8% NaCl SHR only, reaching 17.6 pg/ml at 90 min. The AVP V1 antagonist completely abolished the cold stress-induced rise in MAP in SHR. Thus SHR on a high-NaCl diet have an enhanced pressor response to acute cold exposure compared with SHR on a normal NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 265 (3) ◽  
pp. R689-R696 ◽  
Author(s):  
D. E. Allen ◽  
M. Gellai

Renal alpha 2-adrenoreceptors modulate the hydrosmotic action of arginine vasopressin (AVP) through suppression of AVP-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Circulating catecholamines, likely candidates for the endogenous ligand, are elevated during cold exposure (CE). These studies therefore tested the hypothesis that the diuresis observed with acute CE in rats is due in part to modulation of AVP's tubular action via alpha 2-adrenoceptor activation. Subjects were five male Brattleboro homozygous diabetes insipidus (DI) rats (358 +/- 8 g) receiving chronic AVP replacement (1 microgram.kg-1 x day-1) and seven Long-Evans (LE) normal rats (395 +/- 5 g). In a CE protocol, baseline measurements at room temperature (RT, 24 +/- 0.3 degrees C) were followed by 60-min exposure to 5 +/- 0.5 degrees C. Results were compared with those from a RT time control protocol. The selective alpha 2-antagonist yohimbine (YOH; 10 micrograms.kg-1 x min-1) or vehicle (VEH) was infused throughout the CE and RT protocols. In VEH-infused rats, CE increased urine flow by 63 +/- 12 (DI rats) and 31 +/- 4 microliters.min-1 x 100 g body wt-1 (LE rats), and mean arterial pressure by 36 +/- 1 (DI rats) and 32 +/- 2 mmHg (LE rats). The increased flow was largely a water diuresis, with changes in free water clearance averaging 45 +/- 11 (DI rats) and 28 +/- 3 microliters.min-1 x 100 g body wt-1 (LE rats). YOH treatment completely blunted the cold-induced diuresis in both strains but did not alter the CE-induced hypertension. Glomerular filtration rate was not affected by either CE or YOH infusion.(ABSTRACT TRUNCATED AT 250 WORDS)


1982 ◽  
Vol 100 (2) ◽  
pp. 216-220 ◽  
Author(s):  
Mary L. Forshing ◽  
M.J. Brimble ◽  
R. J. Balment

Abstract. Oxytocin administration in rats infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin dificiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.


1980 ◽  
Vol 60 (3) ◽  
pp. 677-681 ◽  
Author(s):  
A. L. SCHAEFER ◽  
B. A. YOUNG

The influence of acute and chronic cold exposure on the distribution of cardiac output to the gastrointestinal tract was measured in adult sheep (35–50 kg) using radioactive microspheres containing 141Ce and 113Sn. Groups of four sheep were exposed in controlled temperature chambers to either (1) control temperature, 18 °C for 10–12 wk; (2) acute cold, exposure to 3 °C for 12 h; (3) chronic cold, exposure to 3 °C for 10–12 wk. In the control, acute cold and chronic cold treatments, respectively, 26.4, 20.5 and 19.4% of cardiac output was distributed to the gastrointestinal tract. The estimated amount of blood flow (mL/100 g wet tissue/min) to the total gastrointestinal tract was not significantly different among the three treatment groups (67 mL/100 g/min for the control versus 62 and 50 mL/100 g/min, respectively, for the acute cold and the chronic cold sheep). However, there was a significant decrease in blood flow to the reticulo-rumen of the acute cold- and chronic cold-exposed sheep (34.0 and 37.8 mL/100 g wet tissue/min for the acute and chronic cold sheep versus 56.0 mL/100 g/min for the control sheep). The redistribution of gastrointestinal blood flow induced by exposure to cold may be a factor in reduced nutrient absorption in cold-exposed ruminants.


Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 273
Author(s):  
Marc Schargus ◽  
Catharina Busch ◽  
Matus Rehak ◽  
Jie Meng ◽  
Manuela Schmidt ◽  
...  

The aim of this study was to compare the efficacy of trabeculectomy (TE), single XEN microstent implantation (solo XEN) or combined XEN implantation and cataract surgery (combined XEN) in primary open-angle glaucoma cases, naïve to prior surgical treatment, using a monocentric retrospective comparative cohort study. Intraocular pressure (IOP) and the number of IOP-lowering drugs (Meds) were monitored during the first 24 months after surgery. Further disease progression was monitored using peripapillary retinal nerve fiber layer (RNFL) thickness examinations using spectral domain optical coherence tomography (OCT) as well as visual acuity (VA) and visual field (VF) tests. In the TE group (52 eyes), the mean IOP decreased from 24.9 ± 5.9 to 13.9 ± 4.2 mmHg (p < 0.001) and Meds decreased from 3.2 ± 1.2 to 0.5 ± 1.1 (p < 0.001). In the solo XEN (38 eyes) and the combined XEN groups, the mean IOP decreased from 24.1 ± 4.7 to 15.7 ± 3.0 mmHg (p < 0.001) and 25.4 ± 5.6 to 14.7 ± 3.2 mmHg (p < 0.001), while Meds decreased from 3.3 ± 0.8 to 0.8 ± 1.2 (p < 0.001) and 2.7 ± 1.2 to 0.4 ± 1.0 (p < 0.001), respectively. The VF and VA indices showed no sign of further deterioration, the RNFL thickness further decreased in all treatment groups after surgery. TE and XEN led to comparable reductions in IOP and Meds. Although the VA and VF indices remained unaltered, the RNFL thickness continuously decreased in all treatment groups during the 24-month follow-up.


1964 ◽  
Vol 206 (2) ◽  
pp. 425-430 ◽  
Author(s):  
H. Valtin ◽  
H. A. Schroeder

Familial hypothalamic diabetes insipidus ( DI) has arisen as an apparently spontaneous mutation from a strain of Long-Evans hooded rats being bred for unrelated researches not involving radioactivity. The DI rats decrease water intake and urine flow, and increase urine osmolality in response to injected vasopressin. They concentrate their urines only minimally or not at all in response to dehydration, hypertonic saline, nicotine, or stress, and their serum osmolalities and sodium concentrations are significantly higher than those of normal animals. They show marked diminution of neurosecretory material in the neurohypophysis and supraoptic nucleus. The data suggest that the deficiency causing DI in these rats is a lack or dearth of synthesis of vasopressin or its carrier protein, or both.


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