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J Orloff

Publications and source records attributed to J Orloff.

At least 55 records · Page 3Linked to original sources
PubMed1969

Paths of transtubular water flow in isolated renal collecting tubules.

The cells of perfused rabbit collecting tubules swell and the intercellular spaces widen during osmotic flow of water from lumen to bath induced by antidiuretic hormone (ADH). Ouabain had no influence on these changes. In the absence of net water flow intercellular width was unaffected when tubules were swollen in hypotonic external media. Therefore, during ADH-induced flow widening of intercellular spaces is not a consequence of osmotic swelling of a closed intercellular compartment containing trapped solutes, but rather is due to flow of solution through the channel. Direct evidence of intercellular flow was obtained. Nonperfused tubules swollen in hypotonic media were reimmersed in isotonic solution with resultant entry of water into intercellular spaces. The widened spaces gradually collapsed completely. Spaces enlarged in this manner could be emptied more rapidly by increasing the transtubular hydrostatic pressure difference. In electron micrographs a path of exit of sufficient width to accommodate the observed rate of fluid flow was seen at the base of the intercellular channel. It is concluded that the intercellular spaces communicate with the external extracellular fluid and that water, having entered the cells across the luminal plasma membrane in response in ADH, leaves the cells by osmosis across both the lateral and basilar surface membranes.

Animals↗
PubMed1969

Effect of adrenal steroid hormones on the response of the toad's urinary bladder to vasopressin.

This study was designed to examine the effect of adrenal steroid hormones on the response of the toad bladder to vasopressin. Aldosterone enhanced the short-circuit current response, the osmotic water flow response, and the urea permeability response to vasopressin. Since aldosterone also enhanced the short-circuit current response and the osmotic water flow response to adenosine 3',5'-monophosphate, the steroid effect on the bladder's response to vasopressin appears to be at a step beyond the stimulation of adenyl cyclase. Indirect evidence was obtained that the effect of adrenal steroid hormones on the osmotic water flow response to vasopressin is mediated by a different hormone-tissue interaction than that mediating the effect of adrenal steroid hormones on sodium transport. In experiments with three different pairs of mineralocorticoid and glucocorticoid analogues, the former had a greater effect on short-circuit current, the latter on the osmotic water flow response to vasopressin. In addition, the spirolactone SC-14266 markedly inhibited the short-circuit current effect of dexamethasone and had little or no inhibitory effect on the dexamethasone enhancement of the osmotic water flow response to vasopressin. Aldosterone and dexamethasone stimulate the oxidation by the bladder of glucose-6-(14)C and depress the rate of oxidation of glucose-1-(14)C compared with glucose-6-(14)C. SC-14266 inhibited the effect of dexamethasone on the oxidation of glucose-6-(14)C but did not alter the effect of the steroid on the rate of oxidation of glucose-1-(14)C compared with glucose-6-(14)C, suggesting that the latter is a glucocorticoid effect and the stimulation of glucose-6-(14)C oxidation a mineralocorticoid effect. Under conditions in which aldosterone has produced a marked enhancement of short-circuit current and the permeability response to vasopressin, the steroid had no detectable effect on cell water content or on cell sodium, potassium, or chloride.

Aldosterone↗
PubMed1968

Ultrastructural studies of vasopressin effect on isolated perfused renal collecting tubules of the rabbit.

Isolated cortical collecting tubules from rabbit kidney were studied during perfusion with solutions made either isotonic or hypotonic to the external bathing medium. Examination of living tubules revealed a reversible increase in thickness of the cellular layer, prominence of lateral cell membranes, and formation of intracellular vacuoles during periods of vasopressin-induced osmotic water transport. Examination in the electron microscope revealed that vasopressin induced no changes in cell structure in collecting tubules in the absence of an osmotic difference and significant bulk water flow across the tubule wall. In contrast, tubules fixed during vasopressin-induced periods of high osmotic water transport showed prominent dilatation of lateral intercellular spaces, bulging of apical cell membranes into the tubular lumen, and formation of intracellular vacuoles. It is concluded that the ultrastructural changes are secondary to transepithelial bulk water flow and not to a direct effect of vasopressin on the cells, and that vasopressin induces osmotic flow by increasing water permeability of the luminal cell membrane. The lateral intercellular spaces may be part of the pathway for osmotically induced transepithelial bulk water flow.

Animals↗
PubMed1968

Effect of prostaglandin E1 on the permeability response of the isolated collecting tubule to vasopressin, adenosine 3',5'-monophosphate, and theophylline.

The effect of prostaglandin E(1) (PGE(1)) on the water permeability response to vasopressin, theophylline, and cyclic adenosine 3',5'-monophosphate (C-AMP) of isolated, perfused collecting tubules of the rabbit was investigated in vitro. Prostaglandin is a naturally occurring substance present in a number of tissues, including kidney. It has been implicated in the action of a variety of hormones, many of which are known to exert their physiological effects through the intermediacy of the C-AMP system. In the collecting tubule, PGE(1) (10(-7) M) elicited a minimal increase in net water absorption along an osmotic gradient. However, when administered in association with a concentration of vasopressin (2.5 muU ml(-1)) selected to induce a submaximal increment in water absorption, the effect of the latter was reduced by approximately 50%. Theophylline (5 x 10(-3) M) also increased net water absorption, an effect not previously demonstrated in renal tissue. This effect was potentiated by the simulataneous addition of PGE(1). In contrast, PGE(1) did not influence the increase in net water absorption induced by C-AMP (10(-2) M). Since C-AMP is responsible for the permeability effects of vasopressin in renal tissue, the present results are consistent with the view that PGE(1) interferes with the action of the octapeptide by competing with it at a site which influences the generation of C-AMP. In addition it is proposed that prostaglandin may be an important modulator of the action of vasopressin. The tubule is exquisitely sensitive to the hormone, responding to as little as 0.25 muU ml(-1). It is conceivable that in the intact animal prostaglandin may serve to dampen the effects of small amounts of residual hormone and thereby prevent overshoots in permeability which might otherwise occur.

Animals↗
PubMed1968

Control of fluid absorption in the renal proximal tubule.

Glomerulotubular balance was investigated in isolated, perfused rabbit proximal tubules in vitro in order to evaluate some of the mechanisms proposed to account for the proportionate relationship between glomerular filtration rate and fluid absorption generally observed in vivo. The rate of fluid transport from lumen to bath in proximal convoluted tubules in vitro was approximately equal to the estimated normal rate in vivo. The absorption rate in proximal straight tubules however was approximately one-half as great. If the mechanism responsible for maintenance of glomerulotubular balance is intrinsic to the proximal tubule, as has been proposed on the basis of micropuncture studies, the rate of fluid absorption in vitro should be directly related to the perfusion rate and/or tubule volume. In the present studies absorption rate was only minimally affected when perfusion rate was increased or the tubule distended. Thus, glomerulotubular balance is not mediated by changes in velocity of flow of the tubular fluid or tubular diameter and therefore is not an intrinsic property of the proximal tubule. It has also been proposed that glomerulotubular balance results from a humoral feedback mechanism in which angiotensin directly inhibits fluid absorption by the proximal convoluted tubule. In the present experiments, angiotensin was found to have no significant effect on absorption rate.

Absorption↗