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K D Mitchell

Publications and source records attributed to K D Mitchell.

46 records · Page 3Linked to original sources
PubMed1988

Angiotensin influences on tubuloglomerular feedback mechanism in hypertensive rats.

The tubuloglomerular feedback (TGF) mechanism was evaluated in the nonclipped kidney of Goldblatt hypertensive rats from both stop flow pressure (SFP) and single nephron glomerular filtration rate (SNGFR) responses to step increases in late proximal perfusion rate from 0 to 40 nl/min. During control conditions, increases in late proximal perfusion rate produced flow dependent decreases in SFP and SNGFR with maximal values of 10.2 +/- 1.0 mm Hg and 12.9 +/- 2.5 nl/min, values similar to those obtained in normal rats. During ACE inhibition (MK 422; 0.6 mg/kg/hr), arterial pressure decreased from 168 +/- 8 to 137 +/- 7 mm Hg and there was a marked attenuation in the magnitude of SFP feedback responses (delta = 2.5 +/- 0.3 mm Hg). SNGFR feedback responses, however, were not significantly impaired. Direct decreases in renal arterial pressure reduced control SFP but SFP feedback responses were maintained, indicating that the attenuated SFP feedback responses during ACE inhibition were not due to decreased arterial pressure. Superimposed infusion of angiotensin II during ACE inhibition partially restored SFP feedback responses. In contrast, norepinephrine infusion did not result in a similar restoration of SFP feedback sensitivity. These results indicate that the nonclipped kidney of Goldblatt hypertensive rats has an intact TGF mechanism as assessed from SFP and SNGFR feedback responses. Furthermore, ACE inhibition attenuates SFP but not SNGFR feedback responses, and systemic angiotensin II infusions can restore SFP feedback responsiveness towards normal.

Angiotensin II↗
PubMed1988

Enhanced tubuloglomerular feedback during peritubular infusions of angiotensins I and II.

Experiments were performed in pentobarbital sodium-anesthetized rats to determine whether increases in intrarenal generation of angiotensin II (ANG II) can enhance the sensitivity of the tubuloglomerular feedback mechanism. Stop-flow pressure (SFP) feedback responses to step increases in late proximal perfusion rate were obtained during control conditions and during simultaneous peritubular capillary infusion of either angiotensin I (ANG I) or ANG II. Infusion of either 10(-7) M ANG II or 10(-5) M ANG I, at rates (18.3 +/- 0.9 and 14.8 +/- 1.5 nl/min, respectively) that did not affect resting SFP, enhanced the magnitude of SFP feedback responses both at a low proximal perfusion rate of 10 nl/min (2.9 +/- 0.9 vs. 0.3 +/- 0.2 and 4.5 +/- 1.0 vs. 0.1 +/- 0.1 mmHg, respectively) and at proximal perfusion rates (greater than 30 nl/min) that elicited a maximal feedback response (13.1 +/- 1.0 vs. 10.1 +/- 0.7 and 13.5 +/- 1.6 vs. 9.8 +/- 0.8 mmHg, respectively). With a higher ANG I infusion rate (20 nl/min), control SFP measured in the absence of distal volume delivery decreased from 39.2 +/- 0.6 to 12.0 +/- 2.8 mmHg (n = 18). These effects were blocked when the ANG II receptor antagonist, saralasin (10(-5) M, Sar), was added to the infusate. In addition, the magnitude of the maximal SFP feedback response was not altered during infusion of Sar alone or ANG I + Sar. These findings indicate that ANG II, either added or formed de novo beyond the glomerular circulation, can enhance the sensitivity of the tubuloglomerular feedback mechanism.

Angiotensin I↗
PubMed1987

Superficial nephron responses to peritubular capillary infusions of angiotensins I and II.

Proximal tubular reabsorption, stop-flow pressure (SFP), and single nephron glomerular filtration rate (SNGFR) were measured in the absence of and during infusion of an isotonic saline solution containing either angiotensin I (ANG I; 10(-6) to 10(-5) M) or angiotensin II (ANG II; 10(-9) to 10(-7) M) into an adjacent peritubular capillary at a rate of 20 nl/min. Dilution of the infused ANG I and ANG II occurred in the peritubular capillary blood and as the peptides diffused into the interstitium. Infusion of either 10(-7) M ANG II or 10(-5) M ANG I increased proximal fractional fluid reabsorption (FRH2O) and decreased both SFP and SNGFR. There were no significant changes in FRH2O or SNGFR during infusion of 10(-5) M ANG I when the converting enzyme inhibitor enalaprilat (MK 422, 10(-3) M) was added to the infusate. Similarly, peritubular infusion at lower concentrations of either ANG II (10(-9) or 10(-8) M) or ANG I (10(-6) M) did not alter FRH2O, SFP, or SNGFR. These data indicate that conversion of ANG I to ANG II can occur in the peritubular capillary or interstitial environment and that increases above the normal endogenous levels in the postglomerular interstitial ANG II concentration can enhance proximal tubular reabsorption and increase preglomerular resistance and thereby reduce SNGFR.

Angiotensin I↗
PubMed1986

Sar1-leu8-angiotensin II reverses the effects of captopril on renal function in rats.

In Inactin-anaesthetized rats inhibition of angiotensin converting enzyme by captopril resulted in a small decrease in mean arterial blood pressure accompanied by increases in the rates of glomerular filtration, water and electrolyte excretion. Infusion (100 pmol/min) of sar1-leu8-angiotensin II (sar1-leu8-AII) during continuing converting enzyme blockade reversed these changes in renal function but had no effect on arterial blood pressure. The data indicate that sar1-leu8-AII has partial agonist activity in the kidney although it acts as an antagonist of AII in the systemic circulation. This supports the proposal that angiotensin receptors within the kidney differ from those in the peripheral circulation.

Animals↗
PubMedDate not supplied

Influence of intrarenally generated angiotensin II on renal hemodynamics and tubular reabsorption.

There is growing recognition that angiotensin II (ANG II) formed intrarenally exerts direct effects on renal hemodynamics and tubular reabsorption. In vivo micropuncture experiments performed in anesthetized rats have shown that peritubular capillary infusion of either ANG II or angiotensin I (ANG I), at rates that do not markedly influence baseline vascular resistance, can increase proximal tubular reabsorption rate and enhance the responsiveness of the tubuloglomerular feedback mechanism. With higher ANG II or ANG I infusion rates, pronounced preglomerular vasoconstriction occurs, resulting in reduced glomerular capillary pressure and single nephron glomerular filtration rate. The effects of peritubular capillary infusion of ANG I on glomerular function have been shown to be inhibited by the ANG II receptor antagonist, saralasin, indicating that the observed effects of ANG I on proximal tubular reabsorption and glomerular function are not due to direct effects of the decapeptide but are mediated by increases in the interstitial ANG II concentrations resulting from intrarenally generated ANG II. Interestingly, neither peritubular capillary infusion nor systemic administration of large doses of the angiotensin-converting enzyme (ACE) inhibitor, enalaprilat, elicited significant blockade of the single nephron hemodynamic responses to peritubular infusion of ANG I. These findings indicate that intrarenal conversion of ANG I to ANG II occurs, at least in part, at a site which is inaccessible to acutely administered ACE inhibitors, or that there is an alternative pathway for the intrarenal conversion of ANG I to ANG II that is not blocked by ACE inhibitors.

Absorption↗
PubMedDate not supplied

[Distribution of viruses from the Californian encephalitis serogroup (Bunyaviridae, Bunyavirus) in the northern expanses of Russia].

The study was carried out in 1983-1991 and covered a territory of about 10 x 10(6) km2 in various physico-geographic areas (East Fennoscandia, Northern Russian Plain, West Siberia, Central Siberia, North-Eastern Siberia, and Northern Pacific Region) in the Arctic, Subarctic, Northern-Central-Southern taiga, forest-steppe, and steppe in Northern Russia. A total of 251 strains were isolated from 1391,900 mosquitoes, identified as the California group snowshoe hare (83), Inkoo (44), and Tahyna (2) viruses; 122 strains were not completely identified. Some of the strains with uncommon antigenic composition can be natural reassortants. Fifty-two percent of strains were isolated from Aedes communis and the associate species of mosquitoes, other hosts were A. excrucians (8%), A. cantans (6.25%), A. flavescens (6.25%), A. ciprius (6.25%), A. punctor (4.5%), A. vexans (4.5%), A. cataphylla (3.6%), A. nigripes (3.6%), and A. hexodontus (2.6%). The infection rate of mosquitoes was 0.009% in the tundra, 0.012% in forest-tundra, 0.01% in Northern taiga, 0.02% in Central taiga, 0.017% in Southern taiga, 0.026% in forest-steppe, and 0.097% in steppe. The epidemic season is one month in the tundra (from the beginning of July till the beginning of August), two months in Northern taiga (July-August), and three months in Central taiga (from the second half of June till the beginning of September). The highest infection rate of mosquitoes was observed at the end of the epidemic season in all regions. SSH strains prevailed to the East from the Enisei river, whereas to the West and in the Subarctic regions INK virus predominated, SSH being rare; in the taiga the distribution was quite the opposite. TAH virus was virtually absent. Human morbidity was observed in all territories studied. The immune stratum of adult population is about 30% in the tundra and forest-tundra and about 50% in Northern and Central taiga.

Adult↗