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R H Parsons

Publications and source records attributed to R H Parsons.

14 recordsLinked to original sources

Empty bladder and dehydrated pelvic patch water uptake in Bufo marinus: inhibition by captopril.

Dehydration (10.3 +/- 2.2%, N = 7) caused a significant increase in pelvic patch water uptake (Jv) from 875 +/- 86 (N = 21) to 2130 +/- 150 (N = 21) cm3.cm-2 x 10(-7), while the pectoral Jv increased from 258 +/- 31 (N = 21) to 545 +/- 75 (N = 21 cm3.cm-2 x 10(-7). Captopril inhibited the pelvic patch Jv in empty bladder toads decreasing the Jv from 978 +/- 45 (N = 27) to 607 +/- 38 (N = 27) cm3.cm-2 x 10(-7). In dehydrated toads (15 +/- 2%, N = 14), captopril reduced the pelvic patch Jv from 1807 +/- 213 (N = 21) to 957 +/- 91 (N = 21) cm3.cm-2 x 10(-7). Captopril injection decreased the blood pressure in dehydrated toads from 25.6 +/- 1.9 (N = 21) to 16.9 +/- 1.5 (N = 21) mmHg with no change in heart rate.

Animals↗

Regulation of pelvic patch water flow in Bufo marinus: role of bladder volume and ANG II.

This report examines the importance of bladder volume in regulating cutaneous water uptake (Jv, cm3.cm-2.s-1 x 10(-7)) across the ventral pelvic patch and examines the role of angiotensin II (ANG II) and circulation as the regulatory mechanism. Jv in empty-bladder Bufo marinus (bladder volume 3.89 +/- 1.49%, n = 7) was 1,671 +/- 68 (n = 7). Injection of Ringer solution into the bladder (12.8 +/- 2.2%, n = 7) decreased Jv to 1,025 +/- 202 (n = 7). ANG II injected into toads with filled bladders increased Jv in a dose-dependent manner. At 5 micrograms/100 g toad Jv increased by 136 +/- 63 (n = 6), at 50 micrograms/100 g toad by 432 +/- 82 (n = 7), and at 200 micrograms/100 g toad by 620 +/- 142 (n = 5). Saralasin (200 micrograms/100 g toad) completely inhibited the response to ANG II (50 micrograms/100 g toad) and at 1 mg/100 g toad decreased Jv in empty-bladder toads. These experiments indicate that 1) bladder volume participates in the regulation of Jv in the ventral pelvic patch; 2) ANG II increases the Jv in toads with full bladders; 3) saralasin inhibits the high Jv in empty bladder toads; 4) the high Jv, associated with an empty bladder, requires an intact circulation to be maintained; 5) without an intact circulation, the high water flow associated with an empty bladder causes the Na+ content of the tissue in the ventral patch to be reduced; and 6) ANG II causes only a minimal increases in water permeability in the isolated pelvic patch skin.

Angiotensin II↗

Role of circulation in maintaining Na+ and K+ concentration in pelvic patch in Rana catesbeiana.

Skin samples from the pelvic, pectoral, and back areas of frogs were taken from control (C) animals and from dehydrated animals under three conditions: dehydrated and not exposed to a bathing medium (D), dehydrated live and ventral surface exposed to a bathing medium (DL), and dehydrated with heart stopped and ventral surface exposed to a bathing medium (DHS). The skin concentration of Na+ and K+ of the pelvic patch in the absence of circulation was significantly reduced [DHS 286 +/- 22 microM/mg dry wt (n = 6)] compared with control [C 392 +/- 21 microM/mg dry wt (n = 8)]. However, the pelvic skin concentration was maintained in a frog with an intact circulation [DL 381 +/- 26 microM/mg dry wt (n = 7)] even in the presence of a high pelvic water flow [684 +/- 105 cm3.cm-2.s-1.10(-7) (n = 13)]. The water uptake in the pectoral region [231 +/- 54 cm3.cm-2.s-1.10(-7) (n = 13)] was not high enough to predict a dilution, and none was found. The concentrations were 354 +/- 21 (n = 8), 359 +/- 22 (n = 7), 353 +/- 26 (n = 7), and 373 +/- 45 microM/mg dry wt (n = 6) for C, D, DL, and DHS, respectively. Examination of the Na+ and K+ concentrations separately in the pelvic skin shows that the lower salt content in DHS frogs is mainly due to a loss of Na+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pressure effects on the ADH-induced initiation of water flow in toad bladder.

Earlier studies employed colchicine to demonstrate the need for microtubules in the ADH-induced initiation of increased water permeability in toad bladder. We have used colchicine and hydrostatic pressure together to determine whether formed or growing microtubules are required for initiation of the ADH response in Bufo marinus. When ADH and 8,000 psi were administered simultaneously, the ADH-induced increase in water flow was inhibited while under pressure by 107 +/- 7% (n = 6). Application of 8,000 psi for 10 min before ADH administration resulted in an increased initiation of the ADH osmotic response over the non-pressure-treated control (average acceleration, rate of water flow increase during first 3 min after ADH stimulation, 1.25 +/- 0.27 vs. 0.43 +/- 0.12 mg X cm-2 X min-2, n = 6). In addition, the inhibition of the ADH response brought about by colchicine incubation was overcome with pretreatment of the colchicine-incubated bladders with 8,000 psi for 10 min (average 3-min acceleration, 0.18 +/- 0.04 vs. 1.13 +/- 0.06 mg X cm-2 X min-2, respectively). Repeating the experiments with dibutyryl cAMP gave similar results. We interpret these data as suggesting that growing microtubules are required for initiation. The proposed model is as follows. Pressure removes colchicine inhibition by introducing, through disassembly of formed microtubules, more colchicine-free tubulin subunits. These subunits are then available following decompression to reassemble when the tissue is challenged with hormone.

Animals↗

Bath osmolality: effect on water permeability of epithelial tissue.

When hyperosmotic gradients from 100 to 500 mosM are used to produce a water flux, the water permeability of live and potassium cyanide (KCN)-poisoned frog skin decreases with increasing osmotic gradients. In addition, as the total bath osmolality (corium + epithelial) increases there is a reduction in tissue water. Examination of the tissue cellular and extracellular compartments shows that cell shrinkage caused by the increasing hyperosmolality of the bathing medium correlates with the decrease in osmotic permeability. When the bath osmolality is held constant and cell volume decreases, there is a decrease in the water permeability. High potassium in the external bathing medium causes cell swelling that is associated with an increase in water permeability. These data support the hypothesis that a number of conditions known to affect the water permeability of frog skin do so partly or wholly as a result of a change in the cell volume, which either directly or indirectly alters the osmotic permeability of a rate limiting barrier, possibly the cell membrane.

Animals↗

Nocodazole inhibition of the vasopressin-induced water permeability increase in toad urinary bladder.

Nocodazole is a synthetic antitumor drug that binds rapidly to tubulin. When this drug is applied to toad bladder prior to vasopressin stimulation it inhibits the vasopressin response. A maximum inhibition (68%) is reached with a dose level of 10 micrograms/ml applied one-half hour prior to vasopressin stimulation (20 mU/ml). This compares with an inhibition of 50% seen with a 3-h exposure of the tissue to colchicine (0.1 mM) prior to stimulation with vasopressin. Application of nocodazole (1 microgram/ml) 3 min after hormonal stimulation shows no inhibition of the response at one-half hour past stimulation. These data support the view that microtubules are involved in the vasopressin-induced increase in water permeability in toad bladder and also indicate that this involvement is limited to the period prior to or directly after stimulation.

Animals↗

Water movement across split frog skin.

A net inward fluid reabsorption (salt-linked flow) has been observed in isolated skin epithelium (split skin) with the same magnitude as in whole skin when identical NaCl Ringer solutions were used to bathe both sides. Split skins also respond to a hyperosmotic sucrose solution bathing the outer (epithelial) surface by generating an outward osmotic flow. A non-linear relationship between osmotic flow and the osmotic gradient has been found in split skin similar to that found in whole skin.

Animals↗

Permeability of the diaphragm and fluid resorption from the peritoneal cavity in the rat.

The ability to remove fluid from the peritoneal cavity is greatly impaired in rats after sealing the diaphragm (abrading such that fibrous tissue forms). The in vivo resorptive capacity of rats with sealed diaphragms was significantly reduced from 12.3 +/- 1.77% . hr-1 in controls to 5.05 +/- 2.53% . hr-1 in rats with sealed diaphragms. The in vitro permeability of isolated diaphragms for mannitol, inulin, and dextrans of mol wt 16,000 and 75,000 was 4.69 +/- 0.74, 1.16 +/- 0.22, 0.54 +/- 0.11, and 0.22 +/- 0.04 cm . sec-1 . 10(-6) for controls, and 0.54 +/- 0.24, 0.19 +/- 0.19, 0.09 +/- 0.03, and 0.08 +/- 0.02 cm . sec-1 . 10(-6) for sealed diaphragms, respectively. The reduction in the permeability of the fibrosed diaphragm to larger molecules could account for the reduced resorptive capacity.

Absorption↗

Circulatory effects on osmotic water exchange in Rana pipiens.

Tritiated water (3H2O) exchange was shown to be more sensitive to circulatory changes than to arginine vasopressin (ADH)-induced permeability changes. Reducing the circulation (sciatic artery ligation) and increasing the circulation (severing the sciatic nerve) caused the 3H2O exchange in frog legs to decrease from 6.0 +/- 1.3 (5) to 3.5 +/- 0.5 and increase from 6.0 +/- 0.7 (10) to 8.6 +/- 0.6 ml.h-1, respectively. In contrast injection of ADH caused a negligible increase in 3H2O exchange from whole frogs, while at the same time causing a significant increase in osmotic water exchange from 0.22 +/- 0.08 (6) to 0.63 +/- 0.13 (6) g.100 cm-2.h-1.200 mosM-1. Circulatory changes in whole frogs were produced by inducing a diving bradycardia that was less pronounced in a bath aerated with oxygen than with air. The bradycardia caused a reduction in skin circulation, as measured by 3H2O exchange, from 0.210 +/- 0.007 (16) to 0.17 +/- 0.006 (16) ml.h-1.cm-2 in air mixed media and from 0.149 +/- 0.009 (16) to 0.135 +/- 0.011 (16) in oxygen mixed media. Diving bradycardia was also found to affect osmotic water uptake which decreased from 0.61 +/- 0.05 (16) to 0.39 +/- 0.03 (16) g.100 cm-2.h-1.200 mosM-1 in air mixed media and from 0.61 +/- 0.05 (16) to 0.51 +/- 0.04 (16) in oxygen mixed media. The results indicate that circulation affects osmotic water exchange.

Animals↗

Evidence of nitric oxide and angiotensin II regulation of circulation and cutaneous drinking in Bufo marinus.

The nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME) increased vascular resistance (VR) 10% above baseline of 3.08+/-0.08 (n=11) mmHg/mL/min at 10 mg/kg and 20% above 3.05+/-0.08 (n=9) at 50 mg/kg in anesthetized toads (Bufo marinus). Blood pressure was unaffected by either dose of L-NAME. Blood flow decreased at the higher dose of L-NAME. L-arginine (300 mg/kg) reversed the effects of L-NAME on VR and blood flow in toads treated with 10 mg/kg but not with 50 mg/kg. Injection of 50 mg/kg L-NAME into empty-bladder toads produced a 10% decrease in water uptake, J(v), resulting in a J(v) of 1,267+/-11 cm(3)/cm(2)/s x 10(-7) (n=9) compared to 1,385+/-12 (n=8) for controls. Injection of 10 microg/kg angiotensin II (ANG II) increased J(v) 15% across the pelvic patch (J(v), cm(3)/cm(2)/s x 10(-7)), resulting in a J(v) of 1,723+/-12 cm(3)/cm(2)/s x 10(-7) (n=8) compared to 1,471+/-12 (n=8) for controls. It is hypothesized that during cutaneous drinking blood flow into the capillary bed of the pelvic patch is regulated by nitric oxide and ANG II.

Adsorption↗