Characteristics and outcome profile of hospitalized African patients with COVID-19: The Ethiopian context.

BACKGROUND: The COVID-19 pandemic seems to have a different picture in Africa; the first case was identified in the continent after it had already caused a significant loss to the rest of the world and the reported number of cases and mortality rate has been low. Understanding the characteristics and outcome of the pandemic in the African setup is therefore crucial. AIM: To assess the characteristics and outcome of Patients with COVID-19 and to identify determinants of the disease outcome among patients admitted to Millennium COVID-19 Care Center in Ethiopia. METHODS: A prospective cohort study was conducted among 1345 consecutively admitted RT-PCR confirmed Patients with COVID-19 from July to September, 2020. Frequency tables, KM plots, median survival times and Log-rank test were used to describe the data and compare survival distribution between groups. Cox proportional hazard survival model was used to identify determinants of time to clinical recovery and the independent variables, where adjusted hazard ratio, P-value and 95% CI for adjusted hazard ratio were used for testing significance and interpretation of results. Binary logistic regression model was used to assess the presence of a statistically significant association between disease outcome and the independent variables, where adjusted odds ratio, P-value and 95% CI for adjusted odds ratio were used for testing significance and interpretation of results. RESULTS: Among the study population, 71 (5.3%) died, 72 (5.4%) were transferred and the rest 1202 (89.4%) were clinically improved. The median time to clinical recovery was 14 days. On the multivariable Cox proportional hazard model; temperature (AHR = 1.135, 95% CI = 1.011, 1.274, p-value = 0.032), COVID-19 severity (AHR = 0.660, 95% CI = 0.501, 0.869, p-value = 0.003), and cough (AHR = 0.705, 95% CI = 0.519, 0.959, p-value = 0.026) were found to be significant determinants of time to clinical recovery. On the binary logistic regression, the following factors were found to be significantly associated with disease outcome; SPO2 (AOR = 0.302, 95% CI = 0.193, 0.474, p-value = 0.0001), shortness of breath (AOR = 0.354, 95% CI = 0.213, 0.590, p-value = 0.0001) and diabetes mellitus (AOR = 0.549, 95% CI = 0.337, 0.894, p-value = 0.016). CONCLUSIONS: The average duration of time to clinical recovery was 14 days and 89.4% of the patients achieved clinical recovery. The mortality rate of the studied population is lower than reports from other countries including those in Africa. Having severe COVID-19 disease severity and presenting with cough were found to be associated with delayed clinical recovery of the disease. On the other hand, being hyperthermic is associated with shorter disease duration (faster time to clinical recovery). In addition, lower oxygen saturation, subjective complaint of shortness of breath and being diabetic were associated with unfavorable disease outcome. Therefore, patients with these factors should be followed cautiously for a better outcome.

Characteristics and outcome profile of Hospitalized African COVID-19 patients: The Ethiopian Context

BackgroundThe COVID-19 pandemic seems to have a different picture in Africa; the first case was identified in the continent after it has already caused a significant loss to the rest of the world and the reported number of cases and mortality rate has been low. Understanding the characteristics and outcome of the pandemicin the African setup is therefore crucial. AimTo assess the characteristics and outcome of COVID-19 patients and to identify determinants of the disease outcome among patients admitted to Millennium COVID-19 Care Center in Ethiopia. MethodsA prospective cohort study was conducted among 1345 consecutively admitted RT-PCR confirmed COVID-19 patients from July to September, 2020. Frequency tables, KM plots, median survival times and Log-rank test were used to describe the data and compare survival distribution between groups. Cox proportional hazard survival model was used to identify determinants of time to clinical improvement and the independent variables, where adjusted hazard ratio, P-value and 95% CI for adjusted hazard ratio were used for testing significance and interpretation of results. Binary logistic regression model was used to assess the presence of a statistically significant association between disease outcome and the independent variables, where adjusted odds ratio, P-value and 95% CI for adjusted odds ratio were used for testing significance and interpretation of results ResultsAmong the study population, 71 (5.3%) died, 72 (5.4%) were transferred and the rest 1202 (89.4%) were clinically improved. The median time to clinical improvement was 14 days. On the multivariable Cox proportional hazard model; temperature (AHR= 1.135, 95% CI= 1.011, 1.274, p-value=0.032), COVID-19 severity (AHR= 0.660, 95% CI= 0.501, 0.869, p-value=0.003), and cough (AHR= 0.705, 95% CI= 0.519, 0.959, p-value=0.026) were found to be significant determinants of time to clinical improvement. On the binary logistic regression, the following factors were found to be significantly associated with disease outcome; SPO2 (AOR= 0.302, 95% CI= 0.193, 0.474, p-value=0.0001), shortness of breath (AOR= 0.354, 95% CI= 0.213, 0.590, p-value=0.0001) and diabetes mellitus (AOR= 0.549, 95% CI= 0.337, 0.894, p-value=0.016). ConclusionsThe average duration of time to clinical improvement was 14 days and 89.4 % of the patients achieved clinical improvement. The mortality rate of the studied population is lower than reports from other countries including those in Africa. Having severe COVID-19 disease severity and presenting with cough were found to be associated with delayed clinical improvement of the disease. On the other hand, being hyperthermic is associated with shorter disease duration (faster time to clinical improvement). In addition, lower oxygen saturation and subjective complaint of shortness of breath and being diabetic were associated with unfavorable disease outcome. Therefore, patients with these factors should be followed cautiously for a better outcome.

Challenges and chicken production status of poultry producers in Bishoftu, Ethiopia.

The study was conducted to evaluate the current status and constraints of chicken production among poultry producers in the study area. A high percentage of poultry producers were male (69.2%) and married (53.8%). More than half had at least a tertiary education (53.8%) followed by those with secondary schooling and a primary education. The average age of poultry producers was 33.2 ± 11.0 years and this ranged from 16 up to 65 yr of age. Among all the producers' samples, 36.5% reared chicks while hens were the largest flock type followed by pullets, chicks, cockerels, and cocks. A large proportion of producers (94.2%) provided supplementary feed to their birds and most (82.7%) of them utilized commercial ration. Mostly, 38.5% of poultry producers provide supplementary feed any time depending upon the amount of feed left in the feeding trough. The 3 biggest challenges to producers were sudden outbreak of disease, the cost of commercial feed, and the lack of availability of day-old chicks.

The Epidemiology of Sleep Quality, Sleep Patterns, Consumption of Caffeinated Beverages, and Khat Use among Ethiopian College Students.

Objective. To evaluate sleep habits, sleep patterns, and sleep quality among Ethiopian college students; and to examine associations of poor sleep quality with consumption of caffeinated beverages and other stimulants. Methods. A total of 2,230 undergraduate students completed a self-administered comprehensive questionnaire which gathered information about sleep complaints, sociodemographic and lifestyle characteristics,and theuse of caffeinated beverages and khat. We used multivariable logistic regression procedures to estimate odds ratios for the associations of poor sleep quality with sociodemographic and behavioral factors. Results. Overall 52.7% of students were classified as having poor sleep quality (51.8% among males and 56.9% among females). In adjusted multivariate analyses, caffeine consumption (OR = 1.55; 95% CI: 1.25-1.92), cigarette smoking (OR = 1.68; 95% CI: 1.06-2.63), and khat use (OR = 1.72, 95% CI: 1.09-2.71) were all associated with increased odds of long-sleep latency (>30 minutes). Cigarette smoking (OR = 1.74; 95% CI: 1.11-2.73) and khat consumption (OR = 1.91; 95% CI: 1.22-3.00) were also significantly associated with poor sleep efficiency (<85%), as well as with increased use of sleep medicine. Conclusion. Findings from the present study demonstrate the high prevalence of poor sleep quality and its association with stimulant use among college students. Preventive and educational programs for students should include modules that emphasize the importance of sleep and associated risk factors.

Nonsteroidal antiinflammatory drugs and acute renal failure in elderly persons.

Renal prostaglandin inhibition by nonsteroidal antiinflammatory drugs (NSAIDs) may decrease renal function, especially under conditions of low effective circulating volume. To evaluate the risk of important deterioration of renal function due to this effect, the authors performed a nested case-control study using Tennessee Medicaid enrollees aged > or =65 years in 1987-1991. Cases were patients who had been hospitalized with community-acquired acute renal failure; they were selected on the basis of medical record review of Medicaid enrollees with selected discharge diagnoses. Information on the timing, duration, and dose of prescription NSAIDs used, demographic factors, and comorbidity was gathered from computerized Medicaid-Medicare data files. Of the 1,799 patients with acute renal failure (4.51 hospitalizations per 1,000 person-years), 18.1% were current users of prescription NSAIDs as compared with 11.3% of 9,899 randomly selected population controls. After control for demographic factors and comorbidity, use of NSAIDs increased the risk of acute renal failure 58% (adjusted odds ratio = 1.58; 95% confidence interval (CI): 1.34, 1.86). For ibuprofen, which accounted for 35% of NSAID use, odds ratios associated with dosages of < or =1,200 mg/day, >1,200-<2,400 mg/day, and > or =2,400 mg/day were 0.94 (95% CI: 0.58, 1.51), 1.89 (95% CI: 1.34, 2.67), and 2.32 (95% CI: 1.45, 3.71), respectively (test for linear trend: p = 0.009). Prescription NSAID use resulted in an estimated 25 excess hospitalizations associated with renal failure per 10,000 years of use. Thus, NSAIDs represent a relatively uncommon but avoidable cause of acute renal failure in frail elderly persons.

The natural history of nephrocalcinosis in premature infants treated with loop diuretics.

PURPOSE: We investigated the natural history of nephrocalcinosis in premature infants treated with furosemide and attempted to identify factors to predict infants most at risk. MATERIALS AND METHODS: We evaluated 13 preterm infants in this longitudinal pilot study. During hospitalization and while receiving a loop diuretic nephrocalcinosis developed in each patient. Patients were divided into groups based on resolution (6) and nonresolution (7) according to spontaneous resolution of nephrocalcinosis at any point during followup. The 2 groups were compared to each other and to a control group. RESULTS: Mean followup after discontinuation of furosemide in the resolution versus nonresolution groups was 10.3 and 7.7 months, respectively. Between the 2 groups there was no significant difference in average gestational age, birth weight, number of days hospitalized or on furosemide, or total furosemide dose. Mean calcium-to-creatinine ratio while receiving furosemide at the time nephrocalcinosis developed was 0.38 in the resolution group but 2.23 in the nonresolution group (p < 0.005). Initial calcium-to-creatinine ratio in age matched infants who did not have nephrocalcinosis was 0.4. Frank renal stones developed in 2 of the 7 patients without resolution and 0 of the 6 with resolution. When nephrocalcinosis resolved, it was at a mean of 5.2 months following discontinuation of the diuretic. CONCLUSIONS: Early data indicate that nephrocalcinosis resolves in approximately 50% of premature infants 5 to 6 months after discontinuation of furosemide. The only factor that appears to be predictive of the infants who will have resolution is the calcium-to-creatinine ratio when nephrocalcinosis is diagnosed. In patients without resolution this ratio is much higher than in age adjusted normal controls, while in those with resolution it appears normal for age.

Dietary fatty acid modulates glomerular atrial natriuretic peptide receptor.

Modification of dietary fatty acid (FA) has been shown to affect the incidence of hypertension and coronary artery disease. We studied whether these effects involve changes in the receptor characteristics of vasoactive substance. Characteristics of atrial natriuretic peptide (ANP) receptors were examined in glomeruli isolated from rats fed a diet containing 5% in weight omega 6, 5% omega 3, 20% omega 6, 20% omega 3 polyunsaturated FA or 20% saturated FA (SFA) for greater than 4 weeks. The FA composition of phospholipids in isolated glomeruli showed an elevation in 20:4 omega 6 (arachidonic acid, AA) in 5% omega 6, 20% omega 6 and 20% SFA, and elevations in 20:5 omega 3 (eicosapentaenoic acid, EPA) in 5% omega 3 and 20% omega 3 groups. The radioligand binding study revealed: (1) in 20% FA group, receptor density (Ro, fmol/mg prot) of ANP was significantly decreased compared to 5% group (262 +/- 13, n = 8 to 120 +/- 13, n = 12) without changes in equilibrium dissociation constant (KD), (2) among high FA (20%) groups, type of FA was essential for determining Ro; higher omega 6 was associated with a lower ANP Ro (177 +/- 11 vs. 103 +/- 3 fmol/mg prot, P less than 0.05) and KD (0.43 +/- .04 vs. 0.27 +/- .02 nM, P less than 0.05). To examine whether the alteration in receptor characteristics is mediated by FA, effects of FA were examined in vitro. In cultured mesangial cells, AA, but not EPA, decreased Ro of ANP receptors (48.7 +/- 4.8% of control, P less than 0.05) without affecting KD.(ABSTRACT TRUNCATED AT 250 WORDS)

Functional significance of leukotriene B4 in normal and glomerulonephritic kidneys.

Leukotriene B4 (LTB4) is the major 5-lipoxgenase product released during early experimental glomerulonephritis. To test its functional relevance, its actions in the normal rat kidney and its influence on renal function in the heterologous phase of mild nephrotoxic serum-induced glomerular injury were examined. Intrarenal administration of leukotriene B4 resulted in mild vasorelaxant and natriuretic responses which were shared by 12(R)-hydroxyeicosatetraenoic acid but not 12(S)-leukotriene B4 or 12(S)-hydroxyeicosatetraenoic acid, suggesting activation of a common recognition site with a requirement for 12(R) stereochemistry. The polymorphonuclear cell-specific activator, N-formyl-Met-Leu-Phe, stimulated leukotriene B4 production from isolated perfused kidneys harvested from nephrotoxic serum-treated rats to a significantly greater degree than from control animals treated with nonimmune rabbit serum. The renal production of leukotriene B4 correlated directly and strongly (r = 0.79, P less than 0.01) with renal myeloperoxidase activity, suggesting interdependence of leukotriene B4 generation and polymorphonuclear cell infiltration. In vivo, intrarenal administration of leukotriene B4 to rats with mild nephrotoxic serum-induced injury was associated with an increase in polymorphonuclear cell infiltration, reduction in renal plasma flow rate, and marked exacerbation of the fall in glomerular filtration rate, the latter correlating strongly with the number of infiltrating polymorphonuclear cells/glomerulus, whereas inhibition of 5-lipoxygenase led to preservation of glomerular filtration rate and abrogation of proteinuria. Thus, although devoid of vasoconstrictor actions in the normal kidney, increased intrarenal generation of leukotriene B4 during early nephrotoxic serum-induced glomerular injury amplifies leukocyte-dependent reductions in glomerular perfusion and filtration rates, likely due to enhancement of polymorphonuclear cell recruitment/activation.

Importance of angiogenic action of angiotensin II in the glomerular growth of maturing kidneys.

We studied the effect of three antihypertensive drugs on the growth of glomeruli in four- to five-week-old Munich-Wistar rats (N = 24), which were undergoing rapid maturation processes. Young rats were given an angiotensin converting enzyme inhibitor (ACEI, enalapril, 50 mg/liter drinking water), verapamil (50 mg/liter) or hydralazine (80 mg/liter) or no treatment for six weeks. Body weight increased comparably in the treatment groups and age-matched controls, reaching on average 197 +/- 11, 214 +/- 12 and 198 +/- 3 g in ACEI-, verapamil- and hydralazine-treated rats, respectively, versus 218 +/- 6 g in control rats. Glomerular hemodynamic patterns, including glomerular capillary pressure, measured in maturing rats after one and six weeks of ACEI treatment were unaffected by ACEI. Mean planar area of glomeruli (PAmean) achieved was smaller than control in ACEI rats (6.60 +/- 0.20 x 10(-3) mm2 vs. 5.37 +/- 0.22, respectively, P less than 0.005), but not in rats treated with other antihypertensive drugs. Furthermore, the maturational PAmean increase in rats given ACEI for six weeks was, on average, only half of that achieved by age-matched controls not given ACEI, in contrast to normal maturational growth with hydralazine or verapamil (29% increase in PAmean from normal baseline in ACEI vs. 52%, 53% and 59% increases in verapamil, hydralazine and control, respectively). In contrast, comparable PAmean values were found in adults with (7.08 +/- 0.22 x 10(-3)mm2, N = 6) and without (6.98 +/- 0.33 x 10(-3)mm2, N = 6) ACEI treatment given for six weeks. Therefore, ACEI, but not verapamil and hydralazine, causes growth retardation in maturing glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired preservation of GFR during hypotension in preexistent renal hypoperfusion.

Autoregulation of renal blood flow and filtration rate was studied using micropuncture technique in Munich-Wistar rats with acute water deprivation (AWD) or congestive heart failure (CHF). In the first set of experiments, reduction of renal perfusion pressure to approximately to 70% of its initial value resulted in uncoupling of glomerular plasma flow rate and single-nephron glomerular filtration rate (GFR) (i.e., disproportionally profound fall in the latter) in AWD and CHF rats, whereas both indices changed little in normal control (NC) rats. The profound decrease in single-nephron GFR in AWD and CHF rats was primarily due to a reduction in glomerular capillary pressure (change from base-line value was -29 +/- 2% in AWD, -27 +/- 1% in CHF, and -8 +/- 2% in NC). This profound fall in glomerular capillary pressure in AWD and CHF rats was associated with a reduction in efferent arteriolar resistance, which contrastingly increased in NC. To investigate the mechanism underlying this unique efferent arteriolar responsiveness in AWD and CHF, the response of renal arterioles to exogenous angiotensin II was examined in separate groups of AWD, CHF, and NC. There was a markedly attenuated efferent arteriolar vasoconstrictive response in AWD and CHF (the change of efferent arteriolar resistance in both groups was some 5% of that in NC). Thus impairment in the ability to preserve GFR in these two conditions is attributed, at least in part, to altered efferent arteriolar response in the face of reduced renal perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of diet, age and sex on the renal response to immune injury in the rat.

We investigated the effect of three factors, namely dietary protein intake, age and sex, on the susceptibility of the renal glomerulus to the binding of antiglomerular basement membrane antibody (anti-GBM) in the early (heterologous) phase of anti-GBM nephritis, and the consequent reduction in glomerular filtration rate (GFR) as measured by inulin clearance (CIn). The effect of diet was examined in approximately equal to 8 week-old female Munich-Wistar rats fed a 40% high (HP) or a 6% low (LP) protein diet, and that of sex and age in male and female rats, 6 week or 10 month old. Following an intravenous dose (3 to 20 micrograms/g body wt) of radiolabeled nephritogenic anti-GBM, assessment of glomerular function was followed by quantitation of anti-GBM binding (values corrected for GBM surface area) in isolated glomeruli. At a given plasma level of antibody, the degree of binding of anti-GBM was slightly but significantly higher in HP than LP-fed rats; the decrease in GFR was significantly more pronounced in HP than LP-fed animals. The amount of anti-GBM binding was significantly greater in adult than young animals; however, the consequent decrease in GFR was more pronounced in the young than adult animals. Sex dependency was not discernible in anti-GBM binding or reduction in GFR. In all of the above experimental groups, the degree of anti-GBM binding was closely correlated with the plasma level of anti-GBM, but not with effective renal plasma flow rate, measured by PAH clearance. Separate groups of rats were subjected to experimental manipulation of single nephron GFR, glomerular capillary hydraulic pressure and glomerular plasma flow rate, by partial aortic constriction and saralasin administration. This set of experiments, using a tracer amount of non-nephritogenic anti-GBM, revealed that glomerular anti-GBM binding is independent of any of the above parameters. The studies indicate that dietary protein intake and age, but not sex, are among the factors determining the susceptibility of the glomerulus to acute immune injury. Since the binding of anti-GBM is determined by the affinity property of the glomerulus per se, and not by the prevailing hemodynamic pattern, the observed dependence of susceptibility to functional impairment on age and protein intake appears to also reflect a property of the glomerulus, which is influenced by age and the degree of dietary protein intake.

In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat.

The effect of prostaglandin I2 and two other vasodilator agents, acetylcholine and sodium nitroprusside, on systemic and renal circulation was studied in 29 adult euvolemic Sprague-Dawley rats. Intra-aortic infusion of prostaglandin I2 (3.6 micrograms/kg/hr; n = 6 rats) produced significant vasodilation (p less than 0.05), as indicated by an average reduction in total peripheral vascular resistance of 24.8 +/- 2.0%, while renal vascular resistance remained essentially unchanged. Essentially identical findings were obtained in a separate group of six rats pretreated with intravenous administration of saralasin (0.5 mg/kg/hr). In contrast, in another group of six rats pretreated with saralasin, intraaortic infusion of acetylcholine (0.35 mg/kg/hr), which caused a reduction in total peripheral vascular resistance (21.4 +/- 3.8%) comparable to that induced by prostaglandin I2, produced a significant fall in renal vascular resistance (average, 27.7 +/- 5.0%) and, hence, an increase in renal blood flow (average, 26.2 +/- 2.9%). The effect of sodium nitroprusside (0.4 mg/kg/hr i.v.) was intermediate between those of prostaglandin I2 and acetylcholine: both renal vascular resistance and total peripheral vascular resistance fell mildly. These results indicate that prostaglandin I2, given in a dose sufficient to cause systemic vasodilation, fails to induce any discernible renal vasodilative response and that this absence of renal vasodilation by prostaglandin I2 in vivo is not due, as previously postulated, to the highly efficient offsetting influence of intrarenal angiotensin II release.

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

To evaluate the pathophysiologic importance of renal nerves in regulating the renal vasomotor tone, we measured several parameters of renal cortical microcirculation before and after acute renal denervation (DNx) in the following three groups of anesthetized Munich-Wistar rats: (group 1) congestive heart failure after surgically induced myocardial infarction (n = 10), (group 2) acute extracellular fluid volume depletion after deprivation of drinking water for 48 h (n = 8), and (group 3) sham or nontreated controls (n = 6). In the myocardial-infarcted rats, DNx led to a uniform increase in glomerular plasma flow rate of, on average, 36%. Single nephron glomerular filtration rate of myocardial-infarcted rats also increased despite a reduction in glomerular capillary hydraulic pressure. These changes were associated with a fall in arteriolar resistances, particularly in the efferent arteriole. The glomerular capillary ultrafiltration coefficient rose in all but one myocardial-infarcted animal. A similar hemodynamic pattern was seen after DNx in water-deprived animals. In every water-deprived animal, glomerular plasma flow rate and single nephron GFR increased on average by 28 and 14%, respectively. Again, afferent and efferent arteriolar resistances decreased significantly. Furthermore, the ultrafiltration coefficient increased uniformly and substantially with DNx. To ascertain the potential importance of the interaction between the renal nerves and angiotensin II in these circumstances, we compared the renal cortical hemodynamics in additional groups of water-deprived rats (group 4) after DNx (n = 15), (group 5) during inhibition of angiotensin II with saralasin (n = 15), and (group 6) during treatment with both saralasin and DNx (n = 15). No appreciable difference was detected between group 4 vs. 6. In contrast, substantial differences were noted between group 5 vs. 6: on average, the glomerular plasma flow rate was 26% higher and the afferent and efferent arteriolar resistances 25% and 27% lower, respectively, in group 6. These observations provide direct evidence to indicate pathophysiologic importance of renal nerves in the profound intrarenal circulatory adjustments in prerenal circulatory impairment. The vasoconstrictive effects of renal nerves appear to be mediated in part by their stimulatory influence on angiotensin II release and their direct constrictor actions on pre- and post-glomerular vessels as well.

Mechanism of preservation of glomerular perfusion and filtration during acute extracellular fluid volume depletion. Importance of intrarenal vasopressin-prostaglandin interaction for protecting kidneys from constrictor action of vasopressin.

Glomerular circulatory dynamics were assessed in 60 adult anesthetized rats, which were either deprived or not deprived of water for 24-48 h. Water-deprived rats (n = 21) were characterized by a depressed level of single nephron glomerular filtration rate (SNGFR) when compared with nonwater-deprived controls (n = 8) (23.2 +/- 1.3 vs. 44.8 +/- 4.1 nl/min). This was primarily due to decreased glomerular plasma flow rate (71 +/- 5 vs. 169 +/- 23 nl/min) and glomerular capillary ultrafiltration coefficient (0.028 +/- 0.003 vs. 0.087 +/- 0.011 nl/[s . mmHg]). Infusion of saralasin to these water-deprived rats resulted in significant increases in plasma flow rate and ultrafiltration coefficient, and decline in arteriolar resistances. Consequently, SNGFR increased by approximately 50% from pre-saralasin levels. When water-deprived saralasin-treated rats were given a specific antagonist to the vascular action of arginine vasopressin (AVP), d(CH2)5Tyr(Me)AVP, a fall in systemic blood pressure occurred, on average from 102 +/- 5 to 80 +/- 5 mmHg, unaccompanied by dilation of renal arterioles, so that both plasma flow rate (129 +/- 8 vs. 85 +/- 13 nl/min) and SNGFR (31.0 +/- 2.9 vs. 18.2 +/- 4.4 nl/min) decreased. This more selective extrarenal constrictor action of AVP was further documented in additional studies in which cardiac output and whole kidney blood flow rate were simultaneously measured. In water-diuretic rats, administration of a moderately pressor dose of AVP (4 mU/kg per min) resulted in a significant rise in kidney blood flow rate (from 8.8 +/- 1.2 to 9.6 +/- 1.3 ml/min). The higher kidney blood flow rate occurred despite a fall in cardiac output (from 111 +/- 7 to 98 +/- 9 ml/min), and was associated with a significant increase in the ratio of systemic vascular to renal vascular resistance (on average from 0.083 +/- 0.014 to 0.106 +/- 0.019). Furthermore, infusion of d(CH2)5Tyr(Me)AVP to water-deprived animals (n = 6) to antagonize endogenous AVP resulted in systemic but not renal vasodilation, so that kidney blood flow rate fell (by approximately 30%), as did systemic-to-renal resistance ratio (by approximately 30%). When the above two experiments were repeated in indomethacin-treated animals, exogenous AVP administration in water-diuretic rats (n = 6) and antagonism of endogenous AVP in water-deprived rats (n = 7) caused, respectively, parallel constriction and dilation in systemic and renal vasculatures. The net effect was unaltered systemic to renal vascular resistance ratio in both cases. These results indicate that (1) unlike angiotensin II, AVP maintains glomerular perfusion and filtration in acute extracellular fluid volume depletion by a more selective constriction of the extrarenal vasculature. (2) The relative renal insensitivity to the vasoconstrictor action of AVP appears to be due to an AVP-induced release of a potent renal vasodilator, sensitive to indomethacin, presumably prostaglandins.