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D W Ploth

Publications and source records attributed to D W Ploth.

At least 37 records · Page 2Linked to original sources
PubMed1984

Evidence for angiotensin-stimulated proximal tubular fluid reabsorption in normotensive and hypertensive rats: effect of acute administration of captopril.

The effects of captopril on mean arterial blood pressure and proximal tubular fluid reabsorption (JV) were examined in anaesthetized normotensive rats and in the non-clipped kidneys of two-kidney, one-clip Goldblatt hypertensive rats. In the normotensive animals, captopril reduced arterial blood pressure from 121 +/- SD 9 to 106 +/- 10 mmHg and JV decreased from 3.78 +/- 0.45 to 2.57 +/- 0.58 X 10(-4) mm3 mm-2 s-1. Captopril had a greater effect on blood pressure in the hypertensive animals (172 +/- 17 reduced to 133 +/- 23 mmHg) although the decrease in JV from 3.62 +/- 0.12 to 2.40 +/- 0.40 was similar to that observed in normotensive animals. These results provide evidence that, in the anaesthetized rat, angiotensin II contributes to the maintenance of the rate of proximal fluid reabsorption. The magnitude of the angiotensin-stimulated component of proximal fluid absorption is similar in normotensive and two-kidney, one-clip Goldblatt hypertensive rats.

Absorption↗
PubMed1983

Angiotensin-dependent renal mechanisms in two-kidney, one-clip renal vascular hypertension.

Our understanding of the physiology of the renin-angiotensin system has advanced remarkably in the last decade as a result of the development of several pharmacologic agents that effectively block components of this humoral cascade. The use of these antagonists has also advanced our understanding of the contribution of the renin-angiotensin system to the development and maintenance of two-kidney, one-clip renal vascular hypertension. These antagonists have contributed greatly to the characterization of the systemic hemodynamic changes that occur in this model and, particularly, to the delineation of the behavior of the nonclipped kidney, a previously normal kidney that is subjected acutely to an environment of elevated systemic blood pressure and the input of a variety of other extrinsic influences. This kidney not only allows the blood pressure to increase and persist at elevated levels but appears to actively participate in the development and propagation of the hypertension. Although a variety of mechanisms impinge on the function of the nonclipped kidney in this model, the goal of this review is to analyze the behavior of this kidney and how its functional state is perturbed, primarily by the influence of angiotensin, which is believed to be delivered to it by the systemic circulation.

Animals↗
PubMed1982

Effects of saralasin infusion on bilateral renal function in two-kidney, one-clip Goldblatt hypertensive rats.

1. Previous studies have shown that administration of converting enzyme inhibitor (CEI, SQ 20 881) to two-kidney, one-clip Goldblatt hypertensive (GH) rats clipped for 3-4 weeks resulted in marked increases in glomerular filtration rate (GFR), water and sodium excretion by the non-clipped kidneys. The clipped kidneys exhibited reduced function that was due, in part, to the reductions in arterial pressure. To evaluate further the hypothesis that the renal responses to CEI were due primarily to the inhibition of angiotensin II rather than other factors, we infused the angiotensin II competitive blocker, saralasin, into GH rats under sodium pentobarbital anaesthesia and examined renal haemodynamics and excretory function of each kidney before and during saralasin infusion and after cessation of saralasin infusion. 2. Saralasin reduced mean arterial blood pressure from 164 +/- 4 to 124 +/- 4 mmHg. Despite the profound fall of arterial pressure, significant increases in renal blood flow from 5.82 +/- 0.22 to 9.15 +/- 0.76 ml/min and glomerular filtration rate from 1.46 +/- 0.10 to 2.18 +/- 0.14 ml/min were observed in the non-clipped kidneys. Renal vascular resistance decreased from 2.34 (+/- 0.14) x 10(5) to 1.17 (+/- 0.19) x 10(5) kPa 1(-1) s [2.34 (+/- 0.14) x 10(6) to 1.17 (+/- 0.19) x 10(6) dyn s cm-5]. Also, concomitant diuresis and kaliuresis and a delayed natriuresis occurred. 3. The clipped kidneys exhibited reductions in renal blood flow, GFR and excretory function during saralasin infusion. 4. Normal rats receiving the identical dose of saralasin responded with a slight but significant decrease in arterial pressure. The increase in renal blood flow and GFR were less than those observed in the non-clipped kidneys of hypertensive rats. 5. These data provide further support to the hypothesis that an angiotensin II-mediated elevation in renal vascular resistance and impairment of renal function exist in the non-clipped kidneys of GH rats.

Angiotensin II↗
PubMed1982

Renal and tubuloglomerular feedback effects of [Sar1,Ala8]angiotensin II in the rat.

Experiments were done in normal rats to assess kidney, single nephron, and tubuloglomerular feedback responses during control conditions and during renin-angiotensin blockade with the angiotensin II (ANG II) antagonist [Sar1,Ala8]angiotensin II (saralasin, 20 micrograms.kg-1.min-1). Plasma renin activity was increased fourfold during saralasin infusion. Glomerular filtration rate (GFR) and renal blood flow increased in parallel from 1.09 +/- 0.04 to 1.26 +/- 0.05 ml/min and from 6.4 +/- 0.5 to 7.6 +/- 0.5 ml/min, respectively. Absolute and fractional sodium excretion were increased sixfold during ANG II blockade. Hydrostatic pressures in proximal tubules, peritubular capillaries, and distal tubules were unchanged. Estimates of nephron GFR (SNGFR) based on collections of distal tubular fluid were increased from 21.6 +/- 1.2 to 24.3 +/- 0.9 nl/min during ANG II blockade. Increases in SNGFR and decreases in fractional absorption at micropuncture sites beyond the late proximal tubule during saralasin administration resulted in increases of flow rate and Cl- delivery at the early distal tubule. Tubuloglomerular feedback activity, assessed by measuring changes in proximal tubule stop-flow pressure in response to alterations in orthograde microperfusion rate from late proximal tubule sites, was significantly attenuated over the range of physiological flow rates for the late proximal tubule during blockade of the renin-angiotensin system. Acute blockade of ANG II in this rat model results in attenuated tubuloglomerular feedback activity and associated changes of hemodynamic and excretory behavior by the kidney.

Angiotensin II↗
PubMed1982

Angiotensin-mediated alterations in nephron function in Goldblatt hypertensive rats.

The present study was performed to evaluate superficial nephron responses of the nonclipped kidney to angiotensin I converting enzyme inhibitor (CEI) (SQ 20,881, 3 mg . kg-1 . h-1) in two-kidney, one-clip Goldblatt hypertensive (GH) rats. Late proximal and early distal tubule collections were obtained before and during CEI. Significant increases in glomerular filtration rate, urine flow, sodium excretion, proximal and distal tubule flow rates, and single nephron glomerular filtration rate (from 24.6 +/- 1.7 to 27.5 +/- 1.6 nl/min) occurred despite reductions in arterial blood pressure (from 160 +/- 5 to 137 +/- 6 mmHg) during CEI. Proximal tubule absolute and fractional reabsorption of fluid, chloride, and total solute decreased significantly. In the nephron segment between the two collection sites, there were increases in absolute but decreases in fractional reabsorption. At the distal tubule level, fractional reabsorption but not absolute reabsorption decreased significantly. Proximal and distal tubule hydrostatic pressures increased significantly while peritubular capillary pressure decreased slightly. Responses following inhibition of angiotensin II formation suggest that there exists an angiotensin II-mediated enhancement in tubular reabsorption in the nonclipped kidney of Goldblatt hypertensive rats.

Administration, Topical↗
PubMed1982

Renin-angiotensin influences on tubuloglomerular feedback activity in the rat.

We have reviewed the development of Thurau's hypothesis that angiotensin mediates the effector responses of distal tubuloglomerular feedback-induced changes of nephron function. Several studies attempting to correlate responsiveness of the tubuloglomerular feedback system with intrarenal renin or juxtaglomerular renin contents have not delineated angiotensin's role in the feedback control system. Others and our own recent studies that have assessed the effects of acute blockade of the renin-angiotensin system on the responsiveness of tubuloglomerular feedback activity suggest that the effects of angiotensin are most likely a modulating influence on the activity of the system rather than the mediator of feedback-induced changes in glomerular function.

Angiotensins↗
PubMed1981

Role of feedback mechanism in renal autoregulation and sensing step in feedback pathway.

The unique morphology of the juxtaglomerular complex has resulted in many investigations evaluating its potential physiological roles. One hypothesis that has stimulated considerable interest is that feedback signals originating from distal tubule cells, presumably at the macula densa segment, participate in the phenomenon of renal autoregulation. Data obtained from dog experiments indicate tha autoregulation of single nephron glomerular filtration rate (SNGFR) is most consistently observed when fluid delivery to the early distal tubule is not interrupted. In contrast, techniques that interfere with normal orthograde fluid delivery to the distal nephron have usually resulted in increases in SNGFR and an inability to exhibit appropriate autoregulatory responses to decreases in arterial pressure. There is considerable uncertainty concerning the nature of the intraluminal component of the early distal tubule fluid responsible for initiating feedback responses. The studies reported in this paper have indicated that feedback mediated decreases in stop-flow pressure and SNGFR in response to increases in distal microperfusion rate can occur with a variety of artificial perfusion solutions, including solutions that contain low concentrations of chloride, sodium, or total electrolytes. Microperfusion studies in the rat have demonstrated that feedback mediated decreases in stop-flow pressure can occur in the absence of associated increases in distal tubule fluid chloride concentration. These results are consistent with the concept that some function of distal tubule fluid osmolality or distal tubule solute delivery may participate in the initiation of feedback signals.

Animals↗
PubMed1980

Impaired autoregulatory responses in contralateral kidneys of two-kidney, one-clip hypertensive rats.

1. Micropuncture and clearance experiments in two-kidney, one-clip renal vascular hypertensive rats examined the ability of the kidney contralateral to renal vascular stenosis to maintain renal function during conditions of reduced renal arterial blood pressure. 2. At their respective spontaneous blood pressures, renal vascular resistance was higher and glomerular filtration rate (GFR) and renal blood flow were not different in the contralateral kidneys of the hypertensive rats (170 +/- 5 mmHg) compared with normal animals (129 +/- 1 mmHg). Urine flow and absolute and fractional excretion of electrolyte were greater from the kidneys of the hypertensive animals. However, pressures in cortical structures were similar in the two groups. 3. As blood pressure was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in renal vascular resistance that failed to allow GFR, renal blood flow or pressures in cortical structures to be maintained. In contrast, normal rats efficiently autoregulated renal vascular resistance to allow GFR, renal blood flow and cortical pressures to be unchanged as blood pressure was altered between 130 and 115 mmHg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys; at comparable blood pressure these indices of excretory function were not different in the two groups. 4. These observations indicate that the contralateral kidney can maintain normal haemodynamic and glomerular function only at elevated blood pressure and suggest the possibility that the impaired capacity to autoregulate renal resistances may contribute to the maintenance of hypertension observed in this model.

Animals↗
PubMed1979

Hypokalemic rhabdomyolysis and acute renal failure. Occurrence following total parenteral nutrition.

A patient experienced severe hypokalemia in the setting of prolonged nasogastric suction and total parenteral nutrition. Severe rhabdomyolysis and acute renal failure ensued. Review of the literature failed to disclose a similar case of hypokalemic rhabdomyolysis and acute renal failure, although the syndrome has been associated with other causes of hypokalemia, and its pathophysiology has been investigated in experimental models. The morbidity associated with extensive myonecrosis and severe, acute renal failure in this patient indicates that hypokalemia and other electrolyte abnormalities should be aggressively corrected in similar clinical settings.

Acute Kidney Injury↗
PubMed1979

Tubuloglomerular feedback and single nephron function after converting enzyme inhibition in the rat.

Experiments were done in normal rats to assess kidney, single nephron, and tubuloglomerular feedback responses during renin-angiotensin blockade with the converting enzyme inhibitor (CEI) SQ 20881 (E. R. Squibb & Sons, Princeton, N. Y.) (3 mg/kg, per h). Converting enzyme inhibition was documented by complete blockade of vascular responses to infusions of angiotensin I (600 ng/kg). Control plasma renin activity was 12.5+/-2.7 ng angiotensin I/ml per h (mean+/-SEM) and increased sevenfold with CEI (n = 7). There were parallel increases in glomerular filtration rate from 1.08+/-0.05 to 1.26+/-0.05 ml/min and renal blood flow from 6.7+/-0.4 to 7.5+/-0.5 ml/min. During CEI infusion absolute and fractional sodium excretion were increased 10-fold. Proximal tubule and peritubular capillary pressures were unchanged. Single nephron glomerular filtration rate (SNGFR) was measured from both proximal and distal tubule collections; SNGFR based only on distal collections was significantly increased by CEI. A significant difference was observed between SNGFR values measured from proximal and distal tubule sites (6.0+/-1.6 nl/min) and this difference remained unchanged after CEI administration. Slight decreases in fractional absorption were suggested at micropuncture sites beyond the late proximal tubule, whereas early distal tubule flow rate was augmented by CEI. Tubuloglomerular feedback activity was assessed by measuring changes in proximal tubule stop-flow pressure (SFP) or SNGFR in response to alterations in orthograde microperfusion rate from late proximal tubule sites. During control periods, SFP was decreased 11.2+/-0.4 mm Hg when the perfusion rate was increased to 40 nl/min; during infusion of CEI, the same increase in perfusion rate resulted in a SFP decrement of 6.7+/-0.5 mm Hg (P<.001). When late proximal tubule perfusion rate was increased from 0 to 30 nl/min, SNGFR was decreased by 15.0+/-1.2 nl/min during control conditions, and by 11.3+/-1.3 nl/min during CEI infusion. Attenuation of feedback responsiveness during CEI was also observed at lower perfusion rates with both techniques. These results indicate that blockade of the renin-angiotensin system with CEI reduces the activity of the tubuloglomerular feedback mechanism which may mediate the observed renal vasodilation.

Angiotensin I↗