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V Kon

Publications and source records attributed to V Kon.

64 records · Page 4Linked to original sources
PubMed1986

Role of peritubular capillary forces in the renal action of carbonic anhydrase inhibitor.

Micropuncture study was performed in Munich-Wistar rats to assess peritubular capillary Starling forces in renal superficial cortex during suppression of proximal fluid reabsorption by carbonic anhydrase inhibitor. Administration of benzolamide (2 mg/kg/hr, i.v., Group 1, N = 7 rats) caused not only reduction in absolute rate of proximal fluid reabsorption (APR, from 26.7 +/- 4.0 nl/min to 17.7 +/- 3.6, P less than 0.001), but also an increase in peritubular transcapillary hydraulic-pressure difference (from 10.0 +/- 0.5 mm Hg to 15.2 +/- 0.5, P less than 0.001). In a separate group of seven rats (Group 2), these parameters did not change significantly without benzolamide treatment. In Group 1 rats, an attempt was made to nullify the benzolamide-induced reduction in the peritubular capillary net reabsorptive forces by infusing hyperoncotic high-hematocrit blood. Following this treatment, while benzolamide administration was continued, values for APR returned to levels (25.6 +/- 4.8 nl/min) nearly identical to those measured prior to benzolamide administration, in association with a rise in peritubular transcapillary oncotic pressure difference. A separate group of six rats treated in a fashion identical to that of Group 1 showed continued suppression of carbonic anhydrase activity following blood infusion as indicated by low levels of whole kidney bicarbonate reabsorption rate. Peritubular capillary reabsorption coefficient was calculated based on the measured values for Starling forces in Group 1 and were unaffected throughout the study. Continued benzolamide administration alone without the treatment of hyperoncotic blood did not change APR significantly (Group 3, N = 7 rats).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Hormonal regulation of glomerular filtration.

Technological advances within the last decade now permit examination of the effects of various vasoactive substances on glomerular hemodynamics and the filtration process. By modulating the vasomotor tone of the preglomerular and postglomerular arterioles, these substances influence the rate of plasma entering the glomerulus and the pressure within the glomerular capillaries. In addition, hormones appear to influence the permeability of glomerular capillaries by altering the surface area available for filtration.

Angiotensin II↗
PubMed1985

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.

Animals↗
PubMed1985

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.

Adrenergic Fibers↗
PubMed1984

Physiologic basis for the maintenance of glomerulotubular balance in young growing rats.

To examine the physiologic basis of preservation of glomerulotubular balance in young growing animals, we measured the various determinants for fluid transfer across the glomerular and postglomerular capillaries in young (approximately 40 days, N = 8) and adult (N = 8) male Munich-Wistar rats under mild volume expansion. The single nephron (SN) GFR increased by approximately 2.5-fold from young to adult animals. The increase in SNGFR was due to marked rises in both glomerular plasma flow rate (QA) and ultrafiltration coefficient (Kf). The increase in QA was associated with a nearly 60% reduction in afferent and efferent arteriolar resistances. As with SNGFR, the absolute proximal reabsorption rate (APR) increased by some 2.5-fold, indicating preservation of perfect glomerulotubular balance. Of the factors determining peritubular capillary uptake of APR, the mean oncotic pressure difference across the peritubular capillary was similar in young and adult animals. The mean hydraulic pressure difference was also comparable in the two groups. By contrast, the peritubular capillary reabsorption coefficient (Kr) rose markedly and accounted entirely for the increase in peritubular capillary uptake of APR during growth. These results obtained under mild volume expansion indicate that the maintenance of glomerulotubular balance in the growing rat requires harmonious growth of renal microcirculation, that is, glomerular capillary (Kf) and arteriolar (QA) maturation balances the development of peritubular capillary (Kr).

Absorption↗
PubMed1983

Effector loci for renal nerve control of cortical microcirculation.

To determine the effector loci for renal neural vasomotor control, we performed micropuncture measurements before or after renal nerve stimulation and during low- (0.5-1.5 Hz) (LFS) or high- (3-5 Hz) (HFS) frequency nerve stimulation in Munich-Wistar rats. In response to HFS, single nephron glomerular filtration rate decreased on average from 24.1 +/- 4.1 to 10.4 +/- 2.3 nl/min. Although mean glomerular transcapillary hydraulic pressure difference remained essentially constant, HFS led to a marked fall in glomerular plasma flow rate (71.3 +/- 0.9 to 44.1 +/- 10.4 nl/min). The latter was associated with significant increase in both afferent (RA) and efferent (RE) arteriolar resistance, on average by more than twofold. Because of this profound arteriolar constriction, early peritubular capillary hydraulic pressure (PEA) fell markedly during HFS (mean: 19.1 +/- 1.4 vs. 13.2 +/- 1.4 mmHg). The ultrafiltration coefficient (Kf) also decreased significantly, on average from 0.055 +/- 0.014 to 0.015 +/- 0.002 nl/(s . mmHg) with HFS. By contrast, LFS affected these indices to a much lesser and more variable degree although the marked decline in PEA was again demonstrated. Despite this decrease in postglomerular capillary hydraulic pressure, absolute proximal tubule fluid reabsorption (APR) failed to change in some animals and decreased slightly in others. Analysis of the Starling forces acting across the peritubular capillaries showed that due largely to a uniform decrease in mean peritubular capillary hydraulic pressure, mean net reabsorption pressure (Pr) rose substantially and significantly, on average by more than 5 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Blood flow dependence of postglomerular fluid transfer and glomerulotubular balance.

The rate of blood flow entering a capillary network can, in some vascular systems, regulate capillary surface area and the rate of fluid and solute transfer. To determine whether such a mechanism exists in the renal peritubular capillary, we performed micropuncture studies in 28 rats during relatively low and high efferent arteriolar blood flow (EABF). High EABF was achieved by intravenous infusion of isoncotic plasma (group 1: from 120 +/- 11 to 301 +/- 49 nl/min [+/- SE]); whole blood with high hematocrit (approximately 75 vol %) (group 2: from 141 +/- 14 to 252 +/- 31 nl/min); or acetylcholine (group 3: from 193 +/- 20 to 266 +/- 26 nl/min). In group 1 rats, plasma infusion caused an increase in single nephron glomerular filtration rate (SNGFR), on average, from 23.2 +/- 2.4 to 45.2 +/- 3.9 nl/min, owing primarily to increased glomerular plasma flow rate (from 63 +/- 5 to 210 +/- 21 nl/min). The rate of fluid uptake by the peritubular capillary, assessed by the absolute rate of proximal fluid reabsorption (APR), also rose significantly, on average from 10.5 +/- 1.2 to 17.5 +/- 2.4 nl/min. This rise in APR was associated with near constancy in mean transcapillary hydraulic (delta Pc) and oncotic (delta IIc) pressure differences, and was therefore attributed to a significant increase in peritubular capillary reabsorption coefficient (Kr), with the mean from 0.017 +/- 0.003 to 0.030 +/- 0.005 nl/(s . mmHg). In group 2 rats, high hematocrit blood infusion led to a significant rise in APR; on average, from 10.7 +/- 0.7 to 15.0 +/- 1.2 nl/min, without changing SNGFR. This rise in APR occurred despite unfavorable changes in the physical forces, namely a significant increase in delta Pc and constancy in delta IIc. Instead, an increase in EABF was again associated with a significant rise in Kr (on average, from 0.016 +/- 0.002 to 0.030 +/- 0.06 nl/[s . mmHg]), which accounted entirely for the rise in APR, independently of SNGFR. In group 3 rats, in which an increase of EABF was induced pharmacologically with acetylcholine, a rise in EABF was also accompanied by a significant increase in Kr, on average, from 0.019 +/- 0.002 to 0.026 +/- 0.004 nl/(s . mmHg). The results indicate that: (a) Kr is modulated by EABF. (b) In view of plasma flow dependence of GFR, blood flow dependence of Kr and APR provides an important basis for glomerulotubular balance.

Absorption↗
PubMed1983

Glomerular mesangium as an effector locus for the tubuloglomerular feedback system and renal sympathetic innervation.

To define the effector loci for the tubuloglomerular feedback system, the determinants of the single-nephron glomerular filtration rate (SNGFR) were assessed in Munich-Wistar rats by direct glomerular puncture during perfusion of Henle's loop with isotonic Ringer's solution at rates of 0 and 40 nl/min. At the higher flow rate, SNGFR averaged only approximately 65% that measured during the lower flow rate. Whereas mean glomerular capillary hydraulic pressure was unaffected, both glomerular plasma flow rate and ultrafiltration coefficient Kf were found to decrease significantly in response to increase in loop perfusion rate, thereby accounting for the measured reduction in SNGFR. These changes were associated with increased afferent (RA) and efferent (RE) arteriolar resistances. Based on the close anatomic contact between mesangial cells and these arterioles, a single effector mechanism channeled through mesangial contractility is suggested to account for the observed reduction in Kf and increase in RA and RE. Mesangial contractility appears to be under sympathetic nerve control. In our recent micropuncture study with Munich-Wistar rats, a marked reduction in SNGFR was observed during high-frequency stimulation (5 Hz) of the renal nerve. This reduction in SNGFR was accompanied by a marked fall in Kf and increase in RA and RE. When kidneys were perfusion-fixed during high-frequency stimulation, a marked reduction in the number of open channels was demonstrated together with marked narrowing of afferent and efferent arterioles. These observations are consistent with the view that sympathetic innervation of mesangium may modulate GFR through its ability to regulate mesangial contractility.

Animals↗