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Biomedical subjects

N Parekh

Publications and source records attributed to N Parekh.

At least 55 records · Page 3Linked to original sources
PubMed1990

Different responses of cortical and juxtamedullary arterioles to norepinephrine and angiotensin II.

Cortical (C) and juxtamedullary (JM) glomerular blood flow were measured with intravitalmicroscopic techniques in the split hydronephrotic kidney of female Wistar rats under Inactin anesthesia. Intravenous injection of small, equivalent pressor doses of norepinephrine (NE) and angiotensin II (Ang II) reduced the diameter of C afferent arterioles by -16 +/- 2.4% and -14 +/- 1.9%, respectively, whereas that of JM afferent arterioles was reduced by only -3.8 +/- 2.7% and -3.8 +/- 1.5%. Blood flow under NE and Ang II was reduced in C glomeruli by -42 +/- 4.9% and -37 +/- 4.0%, respectively, but in JM glomeruli was reduced by -10 +/- 6.2% and -8.6 +/- 2.9% of control. Perfusion pressure reduction during NE or Ang II infusion to preinfusion values revealed autoregulatory behavior only in C glomeruli. In a second series of experiments cyclooxygenase inhibition by local administration of indomethacin (2.8 x 10(-5) M) induced C and JM vasoconstriction. The effects of NE and Ang II during local application of indomethacin were variable but different responsiveness of C and JM vessels disappeared. We assume that the differences in NE and Ang II responsiveness between C and JM vessels under control conditions are caused by a high prostaglandin content or sensitivity, particularly of JM vessels in the hydronephrotic kidney.

Angiotensin II↗
PubMed1990

Effect of anisodamine on the microcirculation of the hydronephrotic kidney of rats.

Anisodamine, an atropine analog, is widely used in China for treatment of acute circulatory shock but mechanisms of its action are not fully known. We investigated the effect of anisodamine on different renal vessels in the hydronephrotic kidney. Anisodamine was added to the tissue bath containing the kidney to produce increasing concentrations from 10(-8) to 10(-3) M. Anisodamine dilated the arcuate artery, interlobular artery and afferent arteriole in a dose dependent manner. The maximal dilation of 15 to 25% in these preglomerular vessels was attained at a concentration of about 10(-5) M. In contrast, the efferent arteriole constricted by about 55% in response to anisodamine. The glomerular blood flow increased by 15 and 40% at anisodamine concentrations of 10(-8) and 10(-5) M respectively. The renal vascular effect of anisodamine could be abolished by the dopamine receptor antagonist haloperidol. Our data indicate that anisodamine is a potent vasodilator of preglomerular renal vessels and that its effect is mediated by activation of the dopaminergic system. The action of anisodamine through a dopaminergic mechanism, as found in the hydronephrotic kidney, may also be involved in its antishock properties.

Acetylcholine↗
PubMed1989

Visualization of renal autoregulation in the split hydronephrotic kidney of rats.

The autoregulatory ability of the renal vascular system in the split hydronephrotic kidney was quantitated with intravital microscopy. The luminal diameters of the arcuate and interlobular arteries as well as the afferent and efferent arterioles were measured. Glomerular blood flow was determined by the dual slit technique. In the first series of experiments, the renal perfusion pressure was reduced by graded clamping of the abdominal aorta. Pressure reduction from 118 mm Hg to 95 mm Hg induced dilation of all preglomerular vessels except for the distal afferent arteriole; there was no change in the efferent arteriole and the blood flow was maintained. Further pressure reductions to 71 and 43 mm Hg caused additional dilations of the preglomerular vessels, a marginal reduction in diameter of proximal efferent arterioles and flow reductions by 15% and 41%, respectively. In the second series, systemic blood pressure was increased by continuous i.v. infusions of norepinephrine (NE). NE constricted pre- and postglomerular vessels except for the distal afferent arteriole; glomerular flow was decreased. Reduction of renal perfusion pressure during NE infusion to the preinfusion value did not diminish glomerular blood flow, but reduced the constrictor response to NE in preglomerular vessels. In a third series of experiments we examined the effect of atrial natriuretic factor (ANF) on renal autoregulation. Addition of ANF (10(-9) to 10(-7) M) to the renal bath induced a dose-dependent dilation of all preglomerular vessels and a constriction of the efferent arteriole. Pressure reduction from 120 to 95 mm Hg resulted in a further preglomerular vasodilation. These experiments demonstrate that autoregulation is mediated primarily by diameter changes in all preglomerular vessels excluding the distal segment of the afferent arteriole. Further, these data suggest that ANF induced dilation of preglomerular vessels does not impair the myogenic response of these vessels.

Acetylcholine↗
PubMed1987

Calcium antagonists preferentially dilate preglomerular vessels of hydronephrotic kidney.

The hydronephrotic kidney of Inactin-anesthetized female Wistar rats was exteriorized in a controlled bath to directly observe preglomerular and postglomerular vessels via television microscopy. Nitrendipine, added to the bath in a concentration that did not alter blood pressure, induced a concentration-dependent dilation of preglomerular vessels. The arcuate artery maximally dilated by 29 +/- 4%, the interlobular artery by 24 +/- 5%, the afferent arteriole near the interlobular artery by 60 +/- 9%, and near the glomerulus by 28 +/- 13%. In contrast the efferent arteriole near the glomerulus dilated by only 11 +/- 6% and near the welling point by 7 +/- 9%. Similarly, diltiazem significantly dilated preglomerular vessels but not efferent arterioles. Acetylcholine significantly dilated all preglomerular vessels and dilated the afferent arterioles near the glomerulus (by 51 +/- 8%) to a greater extent than the calcium blockers. Acetylcholine also significantly dilated the efferent arterioles (near the glomerulus by 26 +/- 5% and near the welling point by 12 +/- 3%). These data suggest that the tone of the preglomerular vessels of the hydronephrotic kidney is more dependent on the entry of extracellular calcium through calcium antagonist-sensitive channels (i.e., potential dependent) than is the tone of the afferent arterioles near the glomerulus and the efferent arterioles.

Acetylcholine↗
PubMed1987

Nitrendipine and the pressure-dependent vasodilation of vessels in the hydronephrotic kidney.

The influence of renal perfusion pressure on the vasodilation of the kidney caused by a calcium antagonist, nitrendipine, was studied. The diameter of several preglomerular and postglomerular vessels in the split hydronephrotic kidney of Inactin-anesthetized rats were measured by in vivo television microscopy. A reduction in the renal perfusion pressure to 80 mm Hg (femoral artery pressure) was achieved by clamping of the aorta above the renal arteries. The pressure reduction induced vasodilation of the arcuate arteries (proximal and distal), interlobular arteries (proximal and distal), and the afferent arterioles near the interlobular arteries. The afferent arterioles at sites near the glomerulus showed no pressure-dependent vasodilation. Topically applied nitrendipine led to a dose-dependent preglomerular vasodilation that did not further increase during perfusion pressure reduction. From these experiments, it is concluded that nitrendipine-induced renal vasodilation is independent of the renal perfusion pressure and primarily caused by its direct effect on preglomerular vessels.

Acetylcholine↗
PubMed1986

Angiotensin II control of the renal microcirculation: effect of blockade by saralasin.

The hydronephrotic rat kidney with intact circulation and innervation was split and spread out as a thin sheet in a tissue bath. The microvasculature was observed in vivo via television microscopy. We quantitated the effects of increasing concentrations (10(-9) to 10(-5) M) of saralasin (angiotensin II antagonist) applied locally in the tissue bath on microvascular diameters and on relative glomerular blood flow (measured using fluorescent labeled RBCs). Saralasin produced an increase in preglomerular diameters which was largest (37 +/- 11%) in the interlobular artery (there was no dilation in the afferent arteriole near the glomerulus), an increase in postglomerular diameters which was largest (17 +/- 4%) in the efferent arteriole near the glomerulus, and an increase in blood flow (19 +/- 4%). If these types of findings would hold for the normal kidney, it would suggest a role for angiotensin II in the control of total renal blood flow, in the regional distribution of flow, and in the control of filtration fraction. We also made control micropressure measurements using the servo-nulling approach. Pressures measured were: afferent arteriole, 65 +/- 5 mm Hg; intraglomerulus, 50 +/- 5 mm Hg; and efferent arteriole, 19 +/- 3 mm Hg. These data indicate that there is major vascular resistance near the glomerulus, especially in the efferent arteriole.

Angiotensin II↗
PubMed1986

Responses of in vivo renal microvessels to dopamine.

The split hydronephrotic kidney preparation was used to directly observe the effects of locally applied dopamine on the in vivo diameters of renal vessels. Dopamine (1 X 10(-6) to 3 X 10(-5) M) produced a concentration-dependent dilation of the arcuate and interlobular arteries and afferent arterioles. Efferent arterioles near the glomeruli also dilated to dopamine but the dilation was less than that of the preglomerular vessels. Higher dopamine concentrations (3 X 10(-4) and 1 X 10(-3) M) produced more variable effects, with a tendency for the arcuate and interlobular arteries and the afferent and efferent arterioles away from the glomeruli to decrease in diameter. After pretreatment with haloperidol, dopamine (1 X 10(-6) to 1 X 10(-4) M) did not dilate any pre- or postglomerular vascular segment, but the tendency for pre- and postglomerular constrictions with higher dopamine concentrations were not abolished. Pretreatment with phentolamine and propranolol enhanced the dilator response of the pre- and postglomerular vessels (except the afferent arterioles near glomeruli and efferent arterioles near welling points) to dopamine (3 X 10(-5) and 1 X 10(-4) M), and abolished the reductions in diameter produced by the high dopamine levels. These data indicate that the dilator effect of dopamine is mediated by interactions with specific dopaminergic receptors, while alpha and beta adrenergic receptors appear to mediate a constrictor influence observed with high dopamine concentrations. The overall effect of dopamine on the renal vessel diameters thus appears to depend on the balance of dilator and constrictor stimuli mediated by multiple receptors.

Animals↗
PubMed1986

Histamine-induced protein leakage in hypertensive rats: inhibition by verapamil.

Hypertension has been associated with an enhanced transport of macromolecules from the vasculature to the interstitium. The first objective of this study was to determine if, under control conditions, there is an enhanced leakage of macromolecules from the cremaster vasculature of the hypertensive rat. The second objective was to determine if the response to a mediator of macromolecular leakage (histamine) was altered in the renovascular hypertensive rat. A third objective was to determine if a calcium entry blocker, verapamil, could inhibit histamine-induced leakage and, if so, was the sensitivity to verapamil different in the renovascular hypertensive rat. Rats were anesthetized with pentobarbital, and the cremaster preparation was used for in vivo television microscopy studies. Fluorescein isothiocyanate was tagged to rat serum albumin (FITC-RSA), and the leakage of this albumin from the vasculature to the interstitium was quantitated by the use of fluorescent microscopy techniques. There was no difference during control conditions in macromolecular leakage between the normotensive and hypertensive rats. However, histamine induced a greater leakage in the renovascular hypertensive rat than in the normotensive controls. In addition, verapamil, in the presence of normal calcium levels, inhibited the histamine-induced leakage in the hypertensive rats but not in the normotensive controls. These data suggest that enhanced macromolecular leakage during hypertension may be due to an increased sensitivity to mediators of protein leakage. These agents may produce protein leakage by enhancing entry of extracellular calcium into endothelial cells.

Animals↗
PubMed1985

Influence of systemically applied angiotensin II on the microcirculation of glomerular capillaries in the rat.

The effect of intravenous infusion of angiotensin II on microvascular parameters of the renal microcirculation of rats was studied. With the aid of fluorescence microscopy and a high sensitivity video system we observed the passage of fluorescence-labeled erythrocytes through single glomerular capillaries on the surface of the rat kidney. From videotaped recordings, we measured the velocity and the flux of erythrocytes using a modified dual-slit technique with support of a microprocessor system. Angiotensin II was administered intravenously at a rate of either 0.2 or 0.4 microgram/min/kg of body wt. Angiotensin II decreased renal blood flow in a dose-dependent fashion (a 32% decrease with 0.2 microgram/min/kg and a 42% decrease with 0.4 microgram/min/kg). The higher rate of angiotensin II infusion had a variable effect on red cell velocity in glomerular capillaries with an overall effect to decrease velocity by 18%. Red cell flux in capillaries was similarly decreased by 25% with angiotensin II infusion. Three successive infusions of angiotensin II did not significantly diminish the effect of the peptide on red cell velocity or flux. Volume flow through the glomerular capillaries (calculated from erythrocyte velocity and vessel diameter) decreased during angiotensin II infusion (0.4 microgram/min/kg) from 3.2 to 2.4 nl/min despite no change in capillary diameter or hematocrit (ratio of erythrocyte flux to volume flow). These data indicate that alterations of the ultrafiltration coefficient (Kf) are not induced by uniform capillary vasoconstriction mechanisms, as others have suggested.

Angiotensin II↗
PubMed1984

Glomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure.

Complete occlusion of the left renal artery for 60 min in the rat produced anuric acute renal failure after 1 day. Using fluorescence microscopy, a television system combined with double slit densitometry, and micropuncture techniques, tubular pressure and tubular flow rates were determined in different segments of superficial nephrons. Intratubular pressures in proximal convolutions of the postischemic kidney were largely heterogeneous due to abnormally increased flow resistance in proximal tubules which were filled with loose obstructive material. Proximal tubular pressure in the control kidney was independent of the site of its measurement and had a mean value of 14.1 mm Hg. In the postischemic kidney pressure decreased gradually along the proximal tubule, its value in the early and late segments being 16.3 and 9.7 mm Hg, respectively. Low pressure in late proximal convolutions excludes a significant flow impediment due to obstruction in more distal segments. The mean nephron filtration rate (SNGFR) obtained by extrapolation of tubular flow data was 62% of the control value, whereas tubular reabsorption was estimated to be 50% above normal. Reduced SNGFR and increased outflux caused a total reabsorption of tubular fluid within 60% of proximal convoluted tubule length. The partial reduction of SNGFR can be explained by increased pressure in early proximal convolutions and reduced glomerular plasma flow known for these kidneys, without postulating a change in glomerular permeability. Tubular obstruction and increased passive outflux in proximal tubules due to cellular damage appear to be crucial mechanisms responsible for the loss of renal function in this model of acute renal failure.

Absorption↗
PubMed1983

Renal oncocytoma associated with diffuse lymphoma.

We report on a sixty-six-year-old man with a poorly differentiated, diffuse lymphoma in whom bilateral multiple renal masses developed six months after starting chemotherapy. Computerized tomography and selective renal arteriograms were suggestive of either recurrence of lymphoma or renal cell carcinoma. Kidney biopsy revealed renal oncocytomas, benign renal tumors. The patient was spared further courses of cytotoxic therapy.

Adenoma↗
PubMed1983

Hydronephrosis: a new method to visualize vas afferens, efferens, and glomerular network.

We have developed a new preparation for in vivo visualization of the glomerular microcirculation, the vas afferens and the vas efferens. This preparation utilizes postischemic hydronephrosis (PIH) to destroy the renal tubular system while preserving a portion of the cortex. In this preparation, glomeruli and associated vasculature remained intact. Observations can be made with either incident light or transillumination. The inner diameter of the vas afferens, measured within 50 microns of the glomerular vascular pole, was 7.9 +/- 0.5 microns (N = 12; SEM) while that of the vas efferens was 7.7 +/- 0.5 microns (N = 12). Both vessels were narrower adjacent to the glomerulus; minimal diameters in this region were 4.5 +/- 0.5 microns (N = 10) and 4.3 +/- 0.5 microns (N = 11), respectively. A specialized round cell, which may act as a sphincter, was seen in the vas efferens. In a second series of experiments, blood velocity was measured in the vas afferens and efferens about 100 microns from the vascular pole. Mean control velocities at these sites were 5.9 +/- 0.9 (N = 14) and 4.6 +/- 1.3 (N = 9) mm X sec-1, respectively; diameters at these same sites were 10.3 +/- 0.6 microns and 11.2 +/- 0.7. During angiotensin II infusion (first series, 0.2 to 0.4 micrograms X min-1 X kg-1, i.v.) the vas efferens in the vicinity of the glomerulus constricted by 22% whereas the corresponding vas afferens showed no consistent response. During angiotensin II infusion, the filtration fraction (GFR/RPF) may, therefore, be elevated by an increased resistance in the vas efferens, particularly at the outflow point of the glomerulus. In the second series of experiments higher dosages of angiotensin II caused vasoconstriction of both vessels, especially at sites more distant from the glomerulus. Furthermore, the new approach is suitable for observing the flow direction within single capillaries of one third to one half of the glomerulus. Therefore, for the first time it is possible to determine the real flow direction in a three-dimensional way.

Angiotensin II↗
PubMed1983

The use of fluorescent labeled erythrocytes for intravital investigation of flow and local hematocrit in glomerular capillaries in the rat.

Fluorescence labeled erythrocytes are suitable markers for red cell velocity and red cell flux through glomerular capillaries in incident light fluorescence microscopy. Mean velocity of the labeled cells was measured from a video recording with a microprocessor using a modified dual slit photometric technic. Red cell flux through the capillary was derived from the labeled cell frequency in capillary flow and systemic concentration of the fluorescent cells. The capillary diameters could be determined after staining plasma with fluorescence labeled dextran. The dynamic hematocrit (HMICRO) was calculated by the ratio of red cell flux to the product of red cell velocity and luminal cross section and varied between +28 and -51% from the corresponding systemic value.

Animals↗
PubMed1981

Intraglomerular microcirculation: measurements of single glomerular loop flow in rats.

With the use of a new fluorescent microscopic technique, we were able to measure the mean intracapillary velocities and pressures of single capillary loops of renal glomeruli of living rats. The technique involved photographing and recording the flow of fluorescent latex particles through the glomerular loops with a television monitor. In 25 rats the single glomerular loop flow velocity was 781 +/- (SD) 271 micrometers . sec-1. The mean diameter of the capillary loops measured 8.4 +/- 1.4 micrometers; their lengths were 72.3 +/- 37.5 micrometers. From the decrease in velocity of flow along the capillary loop, we were able to evaluate the filtration equivalent for the capillary surface. It was possible to measure intracapillary pressures of single glomerular loops continuously under microscopic control. High intracapillary pressures correlated with high intracapillary velocities. From the data we obtained, we were unable to calculate a filtration equilibrium at the ends of the observed capillary loops. For further correlations, we injected the glomeruli we had studied in the living state and examined them with the scanning electron microscope.

Animals↗
PubMed1981

Renal hemodynamics and oxygen consumption during postischemic acute renal failure in the rat.

Acute renal failure in the rat was induced by occluding the left renal artery for 1 hour. The kidneys were examined 1, 3, 10, and 40 days after temporary ischemia. Inulin clearance was essentially zero in oligoanuric kidneys on days 1 and 3, and regained 14% and 63% of the control value on days 10 and 40, respectively. Mean cortical blood flow remained almost constant at 75% of control up to day 10 and normalized subsequently on day 40. Renal oxygen consumption during anuria on days 1 and 3 was 53% and 46% of the control value and increased thereafter concurrently with the restoration of renal function. With a single linear correlation being assumed to exist between sodium reabsorption and oxygen consumption for all kidneys, the sodium reabsorption and oxygen consumption for all kidneys, the sodium transport estimated from oxygen consumption on day 1 was about 40% of control value. The difference between the sodium transport calculated from oxygen consumption and that from inulin clearance decreased with time in the recovery phase. The results indicate only a partial reduction of GFR due to the reduced blood flow in this model. The data are consistent with the hypothesis that tubular leakage and tubular obstruction play an important role in the loss of renal function during the manifestation of acute renal failure.

Acute Kidney Injury↗
PubMed1979

Effects of adrenergic and cholinergic agents on ureteral functions in dogs.

The effects of the autonomic nervous system on ureteral functions were investigated by application of stimulating and blocking drugs. These effects were differentiated from those due to a change of urine flow by perfusing the renal pelvis with isotonic saline. Peristaltic frequency was readily increased by higher flow volume, but was rarely affected by blockage of alpha-adrenergic and cholinergic receptors. The ureteral pacemaker could be activated by alpha-stimulation and inhibited by beta-stimulation. During perfusion of renal pelvis at a pressure of 12 mm Hg, transport capacity of the ureter could be significantly increased either by alpha-blockade or beta-stimulation. Stimulation of alpha-receptors decreased transport capacity, whereas stimulation of cholinergic receptors remained ineffective. These experiments suggest that responses of sympathetic stimulators and blockers are brought about by their influence on ureter muscle tone. The therapeutic value of these drugs is discussed.

Animals↗