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Biomedical subjects

R C Blantz

Publications and source records attributed to R C Blantz.

At least 127 records · Page 7Linked to original sources
PubMed1984

Angiotensin II in adrenergic-induced alterations in glomerular hemodynamics.

UNLABELLED: Micropuncture analysis of glomerular ultrafiltration (SNGFR) was conducted in Munich-Wistar rats to assess the functional responses to moderate-frequency (3-Hz) renal nerve stimulation. Angiotensin II inhibition (ANG II-inhib) was produced by the intravenous administration of [Sar1, Ala8] angiotensin II or MK 421 to investigate whether it modulates the effects of renal nerve stimulation. Micropuncture measurements were obtained before and during renal nerve stimulation. Renal nerve stimulation decreased SNGFR approximately 25% (from 49.9 +/- 2.3 to 38.0 +/- 1.4 nl X min-1 X g kidney wt-1), the result of decreased glomerular capillary hydrostatic pressure gradient and nephron plasma flow. These decreases were due to increased afferent (approximately 43%) and efferent (approximately 30%) arteriolar resistances, since the glomerular ultrafiltration coefficient remained unaffected. The effects of renal nerve stimulation during ANG II-inhib were less in magnitude than in renal nerve stimulation alone: SNGFR decreased from 48.0 +/- 1.5 to 44.8 +/- 2.0 nl X min-1 X g kidney wt-1 after renal nerve stimulation. The net renal production of norepinephrine was augmented by renal nerve stimulation but it was not influenced by ANG II-inhib. IN CONCLUSION: renal nerve stimulation can regulate glomerular ultrafiltration by altering vascular resistances, and angiotensin II appears to be a critical factor for the full functional expression of renal nerve stimulation at the glomerulus.

Angiotensin II↗
PubMed1984

Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats.

We have examined the response of directly and indirectly (stop-flow) measured glomerular capillary hydrostatic pressure (PGC) and single nephron glomerular filtration rate (SNGFR) to increases in late proximal tubular flow rate in hydropenic rats and rats in which angiotensin II (ANG II) and prostaglandin generation was reduced by 3- to 5-day pretreatment with converting enzyme inhibitor (MK-421) and meclofenamate. In control rats, PGC (48 +/- 2 mmHg) decreased 9 +/- 1 mmHg when 25 nl/min was added to late proximal flow in unobstructed tubules, and PGC decreased 9 +/- 1 mmHg when late proximal perfusion rate was increased from 0 to 40 nl/min, incrementally, in wax-blocked tubules. The turning point or half-maximal response for PGC was at perfusion rates of 23 +/- 2 nl/min. Stop-flow estimated PGC (47 +/- 1 mmHg = control) responses were nearly identical. SNGFR decreased from 30 +/- 1 to 21 +/- 1 nl/min with increased perfusion in control rats. In ANG II-prostaglandin-blocked rats, PGC and stop-flow pressure responses were completely eliminated, yet SNGFR response persisted (36.2 to 28.0 nl/min) but to a somewhat lesser extent. Both direct and indirect PGC decrease with increases in late proximal flow rate in untreated rats. Studies in ANG II-prostaglandin-blocked rats suggest that tubuloglomerular feedback SNGFR responses can occur without changes in PGC, possibly via parallel changes in afferent and efferent arteriolar resistances.

Angiotensin I↗
PubMed1983

Determinants of serum 1,25(OH)2D levels in renal disease.

Serum 1,25(OH)2D and factors related to its production were studied in 39 patients with various degrees of renal insufficiency. Serum 1,25(OH)2D levels correlated positively with 1/serum creatinine values (r = 0.54, P less than 0.001) and negatively with serum phosphorus (r = -0.39, P less than 0.02) and age (r = -0.33, P less than 0.05). There was no significant correlation between 1,25(OH)2D levels and serum calcium or calcitonin or PTH, although the logarithm of PTH correlated inversely with 1,25(OH)2D levels (r = -0.47, P less than 0.01). Patients who had normal or supranormal 1,25(OH)2D levels despite low GFR tended to have low serum phosphorus values. Serum levels of bone Gla protein (BGP), a biochemical marker for bone metabolism, correlated negatively with 1/serum creatinine (r = -0.39, P less than 0.02) and positively with PTH (r = 0.57, P less than 0.001) and age (r = 0.33, P less than 0.05). Prophylaxis with 1,25(OH)2D should be considered in patients with significantly decreased serum 1,25(OH)2D levels, as seem to occur when serum creatinine is greater than 4.0 mg/dl. However, despite the statistically significant correlation between serum 1,25(OH)2D and 1/serum creatinine, direct measurement should be used to ascertain the serum concentration of 1,25(OH)2D in chronic renal insufficiency.

Adult↗
PubMed1983

Mechanism of altered glomerular hemodynamics during chronic sodium depletion.

Chronic sodium depletion in the rat is associated with decreased nephron filtration rate (SNGFR), nephron plasma flow (rpf), and a reduction in the glomerular permeability coefficient (LpA). This study was designed to determine whether the reduction in LpA could be acutely reversed with volume repletion and whether administration of angiotensin I converting enzyme inhibitor will restore LpA to normal values in the sodium-depleted rat. Measurements were performed in Munich-Wistar rats employing micropuncture techniques to assess the effects of acute volume repletion, 3-5 days of oral converting enzyme inhibitor (CEI) (30 mg . kg body wt-1 . day-1), and longer term (13-18 days) treatment with CEI begun just before or after initial volume depletion. Volume repletion in chronic sodium-depleted rats restored LpA to normal control values within a 60-min period, and values for glomerular dynamics were not different from a group of normal NaCl-intake rats to which the same treatment was applied. Both short-term and long-term CEI treatment during sodium depletion resulted in restoration of rpf to values not different from those with normal NaCl intake. However, only long-term but not short-term CEI treatment restored LpA to normal values. These studies suggest that intrarenal angiotensin II may mediate this reduction in LpA during chronic sodium depletion, but an effect of adrenergic nerve activity has not been excluded.

Angiotensin II↗
PubMed1983

Renal denervation in the rat: analysis of glomerular and proximal tubular function.

We examined 1) the potential modifications in both single nephron filtration rate (SNGFR) and the determinants of glomerular ultrafiltration, and 2) the alterations in peritubular capillary (PTC) "physical factors" that may contribute to changes in proximal tubular reabsorption (APR) after acute renal denervation (DNx). Micropuncture measurements were obtained in euvolemic Munich-Wistar rats with DNx or sham operation (sham). The content of norepinephrine in renal tissue homogenates was markedly reduced in DNx kidneys compared with sham kidneys (P less than 0.001). Mean arterial blood pressure, hematocrit, whole kidney GFR, and urinary flow rate were not different between the sham and DNx groups. Absolute urinary sodium excretion was 3 times greater in the DNx than in the sham group (P less than 0.01). SNGFR and its determinants were not statistically different in the two experimental conditions. APR was significantly reduced by approximately 25% in DNx (P less than 0.02). This reduction in APR was not accompanied by significant directional changes in peritubular capillary and renal interstitial pressures and the passive driving forces acting across the PTC-proximal tubular epithelium. These data demonstrate that elimination of renal innervation does not alter SNGFR or its determinants and suggest that the effect of denervation on APR is a primary epithelial event that occurs independent of changes in renal interstitial pressure and peritubular oncotic and hydrostatic pressures.

Absorption↗
PubMed1983

Mechanism of diuresis following acute modest hyperglycemia in the rat.

In paired micropuncture studies in the Munich-Wistar rat we examined the mechanism of diuresis after acute induction of modest hyperglycemia (430-460 mg/dl) in the absence of an increase in total body water. The major reasons for the diuresis were an increase in nephron filtration rate (SNGFR) (from 30.3 +/- 1.8 to 35.3 +/- 1.6 nl/min) and a reduction in absolute proximal reabsorption (APR) (from 14.0 +/- 0.6 to 9.8 +/- 1.2 nl/min). All determinants of SNGFR were measured and a reduction in systemic oncotic pressure was the sole reason for the increase in SNGFR; vascular resistances did not change. Late proximal tubular fluid-to-plasma glucose concentration ratio was 0.96 +/- 0.04; therefore, the osmotic effects of unreabsorbed glucose could not account for the reduction in APR. Directly measured net renal interstitial pressure increased by 5 mmHg and the peritubular capillary effective reabsorptive pressure decreased (from 15.5 to 10.9 mmHg) in direct proportion to the reduction in APR, changes that could contribute to the reduction in APR. Equal elevations in glucose concentration in tubule and plasma may have also eliminated effective osmotic pressure gradients for water movement and influenced APR. As a result of increases in late proximal tubular flow rate, loop of Henle tubular reabsorption and absolute tubular reabsorption beyond the distal tubule both increased with hyperglycemia. The major reduction in APR was secondary to altered "physical factors" and osmotic effects of glucose that are not dependent on creation of unfavorable chemical gradients for Na+ reabsorption.

Acute Disease↗
PubMed1983

In vivo actions of angiotensin II on glomerular function.

Investigations in which a variety of experimental approaches were used, i.e., micropuncture techniques, analysis of intrarenal hormonal receptor, and electron microscopic analysis of renal morphology, have substantiated a major role for angiotensin II (AII) within the kidney in the regulation of vascular resistances, glomerular function, and even tubular reabsorption. It is also clear that AII exerts a significant influence on glomerular hemodynamics in a variety of altered physiological and pathophysiological states. Recent studies suggest a rather complex interaction between AII and hormonal and adrenergic effects at the glomerular level. AII may also play an important functional role in the pathogenesis of certain forms of acute renal failure. The specific mechanism whereby AII decreases the glomerular ultrafiltration coefficient, however, remains to be fully elucidated. Although in vitro and in vivo studies have suggested that the glomerular effects of AII may be associated with contraction of glomerular mesangial cells, recent in vivo quantitative evaluation has suggested that a uniform vasoconstriction of glomerular capillaries with proportional reductions in glomerular surface area is probably not the sole mechanism for the AII-induced reductions in glomerular ultrafiltration coefficient.

Angiotensin II↗
PubMed1982

Analysis of adrenergic effects of the anesthetics Inactin and alpha-chloralose.

Renal and systemic adrenergic system responses were examined and compared under conditions of Inactin, a barbiturate, and alpha-chloralose anesthesia in hydropenic Munich-Wistar rats. Base-line plasma norepinephrine and other catecholamine levels were higher in Inactin-anesthetized rats. Norepinephrine was infused to raise blood pressure 15-20 mmHg above base line and plasma norepinephrine was again significantly higher with Inactin. In another group, angiotensin II was infused into the cerebral lateral ventricle in both Inactin- and alpha-chloralose-anesthetized rats, a method of stimulating centrally activated adrenergic output. After central stimulation, mean arterial pressure increased only in alpha-chloralose-anesthetized rats. Micropuncture studies examining systemic and glomerular hemodynamics were performed in alpha-chloralose- and Inactin-anesthetized rats before and after the infusion of phentolamine, an alpha-adrenergic antagonist. Infusion of phentolamine decreased mean arterial pressure to a significantly greater extent in the Inactin-anesthetized rats, suggesting a greater base-line systemic alpha-adrenergic activity with Inactin anesthesia. However, renal afferent and efferent arteriolar resistances were not significantly different after phentolamine, and any trend for resistances to decrease could be explained by autoregulation. Inactin increases systemic adrenergic activity, but renal vascular resistances are not significantly affected by this increased activity.

Anesthetics↗
PubMed1982

Effect of modest hyperglycemia on tubuloglomerular feedback activity.

Tubuloglomerular feedback activity was evaluated in hydropenic rats, using "borrowed," glucose-free hydropenic late proximal tubular fluid as microperfusion solution, and in rats with modest hyperglycemia using both hyperglycemic (glucose-containing) and hydropenic (glucose-free) late proximal fluid as test solutions. Changes in nephron filtration rate (SNGFR) in the same nephron were evaluated in all states at zero and 24.6 nl/min late proximal tubule microperfusion rates (the observed hyperglycemic late proximal flow rate) using a Hampel microperfusion pump. In hydropenia, increased microperfusion rate decreased SNGFR, but in hyperglycemic rats, increased perfusion rate with glucose-containing fluid failed to change SNGFR. But when glucose-free, hydropenic fluid was used, SNGFR decreased numerically less than it did in hydropenia. Renal interstitial hydrostatic pressure increased in hydropenia during hyperglycemia, which may account for part of the inhibition of feedback response. Abolition of tubuloglomerular feedback activity during modest hyperglycemia is due to (1) the effects of glucose in the tubular fluid beyond the late proximal tubule and (2) the extraluminal effects of hyperglycemia on the renal interstitial pressure. These findings may explain the elevated GFR in early diabetes mellitus and excessive urinary volume losses during modest hyperglycemia.

Animals↗
PubMed1981

Glomerular immune injury in the rat: the influence of angiotensin II and alpha-adrenergic inhibitors.

Nephron filtration rate (SNGFR) decreases significantly after the administration of large doses of antiglomerular basement membrane antibody (anti-GBM) as a result of reductions in both nephron (renal) plasma flow (RPF) and the glomerular permeability coefficient (LpA). We have examined the participation of angiotensin II (AII) and alpha-adrenergic activity in this process in paired studies in three groups of Munich-Wistar rats: group 1, control and untreated; group 2, rats receiving continuous infusion of sar1-ala8-AII (1 microgram . kg of body wt-1 . min-1), and AII receptor antagonist; and group 3, rats receiving continuous infusion of phentolamine (27 micrograms . kg body wt-1 . min-1), a dose sufficient to block alpha-adrenergic responses. In group 1, SNGFR decreased from 58 +/- 4 to 35 +/- 6 nl . min-1 . g kidney wt-1 (P less than 0.001) after anti-GMB administration due to reductions in RPF (272 +/- 35 to 170 +/- 52 nl . min-1 . g of kidney wt-1, P less than 0.0001) and LpA (0.13 +/- 0.03 to 0.04 +/- 0.01 nl . sec-1 . g of kidney wt-1 . mm Hg-1, P less than 0.02). In group 2, the sar1-ala8-AII-infused rats. SNGFR decreased to a greater extent than it did in group 1 (P less than 0.01) (55 +/- 2 to 18 +/- 6 nl . min-1 . g of kidney wt-1, P less than 0.005) due to a greater reduction in RPF and a similar decrease in LpA. In group 3, phentolamine infusion prevented the decrease in SNGFR (52 +/- 3 to 52 +/- 4 nl . min-1 . g of kidney wt-1, NS) due primarily to elimination of vasoconstriction and a significantly lesser reduction in LpA (0.10 +/- 0.02 to 0.07 +/- 0.01 nl . sec-1 . g of kidney wt-1 . mm HG-1). There were no morphologic differences after anti-GBM administration that were unique to group 3. Blockade of AII activity does not prevent immune induced vasoconstriction or the reduction in LpA. alpha-Adrenergic blockage (1) prevents acute immune induced vasoconstriction and (2) partially prevents the imune induced reduction in LpA.

Adrenergic alpha-Antagonists↗
PubMed1981

Glomerular immune injury in the rat: effect of antagonists of histamine activity.

The participation of histamine via H1 and H2 receptors, in the alteration of glomerular ultrafiltration consequent to acute glomerular immune injury was evaluated in three groups of Munich-Wistar rats, before and after the administration of large doses of antiglomerular basement membrane antibody (AGBM). Group 1 was the control and was untreated; group 2, rats continuously infused with H1 receptor antagonist diphenhydramine; and group 3, rats receiving continuous infusion of the H2 receptor antagonist cimetidine. In group 1, nephron filtration rate (SNGFR) decreased within 60 min after AGBM from 58 +/- 2 to 32 +/- 5 nl . min-1 . g kidney wt-1 (P less than 0.0005) due to decreases in both nephron plasma flow (RPF) (291 +/- 35 to 119 +/- 23 nl . min-1 . g kidney wt-1) (P less than 0.0005) and the glomerular permeability coefficient (LpA) (0.13 +/- 0.02 to 0.06 +/- 0.01 nl . sec-1 . g kidney wt-1 . mm Hg-1) (P less than 0.01). In group 2, SNGFR decreased similarly with AGBM (59 +/- 2 to 23 +/- 10 nl . mm-1 . g kidney wt-1) (P less than 0.0005) due again to major reductions in RPF and LpA, suggesting no protective effect of H1 receptor blockade. In group 3, control, pre-AGBM values for SNGFR and RPF were lower than they were in groups 1 and 2 due to cimetidine infusion. SNGFR and RPF decreased but to a lesser extent in group 3 (48 +/- 3 to 41 nl . min-1 . g kidney wt-1) (P less than 0.0005). Renal vascular resistance did not change after AGBM in this group but interpretation of this finding is complicated because blood pressure decreased after the antibody administration. LpA decreased in group 3 as in group 1, therefore neither H1 nor H2 receptor antagonist prevented reductions in LpA. The absence of vasoconstriction after AGBM during H2 receptor blockade may have been a nonspecific effect of cimetidine. Histamine plays no major role in AGBM-induced immune injury in the rat and does not prevent a reduction in nephron filtration rate.

Animals↗
PubMed1981

Effects of glomerular filtration dynamics on the glomerular permeability coefficient.

Studies were performed in Munich-Wistar rats (n = 24) to determine if the glomerular permeability coefficient (LpA) is affected by changes in the systemic oncotic pressure (pi A) as well as other determinants of glomerular filtration [nephron plasma flow (RPF) and glomerular hydrostatic pressure gradient (delta P)] and systemic hematocrit (Hct). Multiple regression analysis was used to separate the respective relationships of pi A, delta P, RPF, and Hct to LpA to ascertain whether the correlation of LpA to these variables was direct or mediated by some concurrently changing factor. Three two-period protocols were used to examine the changes of these determinants of filtration: 1) hydropenia to 10% body wt saline expansion (SE), 2) SE to 1% body wt of concentrated rat plasma protein (25 g/100 ml) solution (HP) with removal of 1.5% body wt whole blood, and 3) SE to 1% body wt HP with 2.5% body wt whole blood removed with reinfusion of the removed erythrocytes. Changes in LpA correlated directly with changes in pi A (P less than 0.01) and inversely with delta P (P less than 0.01). There was no direct correlation of LpA to RPF or consistent correlation of LpA to Hct.

Animals↗
PubMed1981

Mannitol.

Mannitol is an osmotic diuretic with properties that suit it to a variety of clinical situations. Despite the paucity of controlled studies that precisely define optimal use, a consensus based on published work and clinical experience may be reached. Mannitol can be used prophylactically, as a diagnostic aid, or as therapy for the oliguric state. The diuretic properties of mannitol are also useful in patients with refractory edema or intoxications by aspirin, barbiturates, or bromide. As an extracellular solute, the drug may ameliorate intracranial hypertension or symptoms of dialysis dysequilibrium. The renal and systemic effects of this versatile agent are discussed.

Acute Kidney Injury↗
PubMed1981

The efferent limb of the tubuloglomerular feedback system.

The effector mechanisms which constitute the efferent limb of the tubuloglomerular feedback system were examined after the administration of benzolamide, a carbonic anhydrase inhibitor, which decreased proximal tubule fluid reabsorption by approximately 8 nl/min and transiently increased delivery of fluid out of the proximal tubule. Since benzolamide administration resulted in a decrease in nephron filtration rate (SNGFR) from 29.2 to 21.1 nl/min, late proximal flow rate returned to control values. If the proximal tubule was blocked after benzolamide by insertion of an oil block, the SGNFR returned towards control values. If a proximal tubule oil block was inserted prior to control measurements, SNGFR did not decrease. These data suggest that benzolamide reduces SNGFR by activating tubulo-glomerular feedback mechanisms secondary to increases in the rate of distal delivery. Analysis of the determinants of glomerular ultrafiltration before and after benzolamide administration revealed that the decrease in SNGFR was solely the result of a decrease in nephron plasma flow secondary to increases in afferent and efferent glomerular arteriolar resistance. No change in either the hydrostatic pressure gradient (delta P) or the glomerular permeability coefficient (LpA) was observed. Continuous infusion in saralasin, an angiotensin II antagonist, prevented the reduction in SNGFR and nephron plasma flow after benzolamide. These studies suggest that changes in nephron plasma flow are involved in a mediating the tubuloglomerular feedback response and that angiotensin II may have a role in the effector mechanism.

Angiotensin II↗
PubMed1980

The glomerulus, passive filter or regulatory organ?

This review summarizes recent evidence that glomerular filtration rate is highly regulated and not merely the passive consequence of uncontrolled renal and non-renal factors. Changes in the rate of nephron plasma flow and, under certain circumstances, the glomerular permeability coefficient are the major determining factors which influence the rate of glomerular ultrafiltration. Recent studies suggest that a variety a hormonal substances, when infused, share the capacity to affect glomerular filtration rate by influencing nephron plasma flow and specifically by decreasing the glomerular permeability coefficient. Angiotensin II appears to be the important "final common pathway" mediating many of these hormonal effects on the glomerular permeability coefficient. Of the hormonal substances examined, only ADH appears to exert an independent effect. Also, in certain normal and altered physiologic states, it has been demonstrated that certain hormonal substances, notably angiotensin II, participate in the active regulation of the rate of glomerular filtration through the capacity to influence and regulate the rate of nephron plasma flow and effect reduction in the glomerular permeability coefficient.

Glomerular Filtration Rate↗