Effects of GABA on acutely isolated neurons from the gustatory zone of the rat nucleus of the solitary tract

Responses of acutely isolated neurons from the rostral nucleus of the solitary tract (rNST) to GABA receptor agonists and antagonists were investigated using whole-cell recording in current clamp mode. The isolated neurons retain their morphology and can be divided into multipolar, elongate and ovoid cell types. Most rNST neurons (97%), including all three cell types, respond to GABA with membrane hyperpolarization and a reduction in input resistance. The GABA(A) receptor agonist muscimol reduces neuronal input resistance in a concentration-dependent manner, whereas the GABA(B) receptor agonist baclofen had no effect on any of the neurons tested. The GABA and muscimol reversal potentials were both found to be -75 mV Both the GABA competitive antagonist picrotoxin and the GABA(A) receptor antagonist bicuculline block the effect of GABA in a concentration-dependent manner. These results suggest that GABA activates all neurons in the rNST and that inhibitory synaptic activity is important in brainstem processing of gustatory and somatosensory information.      

Role of the autonomic nervous system, renin-angiotensin system, and arginine vasopressin during the onset and maintenance of ACTH hypertension in sheep

The roles of the autonomic nervous system, renin-angiotensin system, and arginine vasopressin (AVP) during the onset of ACTH-induced hypertension were investigated in conscious sheep. Autonomic ganglion blockade or combined adrenergic and cholinergic receptor blockade demonstrated that an intact sympathetic nervous system was not essential for the development or maintenance of the hypertension. Autonomic blockade augmented the pressor response to ACTH, indicating that baroreceptor-mediated reflexes normally operate to suppress the degree of hypertension produced by ACTH. Evidence was obtained suggesting that the renin-angiotensin system and AVP may partially contribute to the maintenance of ACTH hypertension in the presence of autonomic blockade. However, the precise mechanism by which ACTH raises arterial pressure remains to be elucidated.     

Haemodynamic and renin responses to prostacyclin infusion in Na depleted and Na restricted sheep

The haemodynamic and renin responses to prostacyclin (PGI₂) infusion were examined in sheep during sodium depletion and dietary sodium restriction. The haemodynamic effects of PGI₂ infusion in sodium depleted and sodium restricted sheep were similar to those obtained in the sodium replete animal. The renin proportionate response to PGI₂ was not altered by sodium restriction but blunted by sodium depletion, compatible with the hypothesis that endogenous PGI₂ is high in Na depletion.     

Replacement of receptor cells in the hamster vomeronasal epithelium after nerve transection

Chemoreceptor cells in the vomeronasal and olfactory epithelium are replaced following experimentally induced degeneration. This study analyzes quantitatively the time course and degree of vomeronasal receptor cell replacement. Unilateral transection of the vomeronasal nerves in adult hamster was used to induce a retrograde degeneration of receptor cells in the vomeronasal organ. Histological measurement of both number of receptor cells and epithelial thickness were made for recovery times from 0 to 60 days. After nerve transection, there was a gradual degeneration of receptor cells, the number decreasing to 50% of control by day 2 and 16% by day 6. During days 7-15 maximum receptor cell replacement was observed. Cell number increased rapidly and reached a peak on day 15. At recovery times of 40-60 days, cell number returned to the control level. Epithelial thickness, however, decreased to 60-70% during the degeneration period (days 4-6) and did not return to control levels. After 40-60 days epithelial thickness remained at 70% of control. These results demonstrate that vomeronasal receptor cells are replaced following degeneration, but epithelial thickness does not return to control levels. These findings suggest that the number of replacement cells is not limited by the reduced thickness of the epithelium, and that recovery mechanisms may function to restore an optimum number of receptor cells.      

The effect of ACTH on the plasma concentrations of the "hypertensinogenic" steroids, 17 alpha-hydroxyprogesterone and 17 alpha,20 alpha-dihydroxy-4-pregnen-3-one in sheep

The plasma concentrations of 17 alpha-hydroxyprogesterone (17 alpha OHP) and 17 a'20 alpha-dihydroxy-4-pregnen-3-one (17 alpha 20 alpha OHP) have been measured in sheep during 5 days of ACTH administration at 20 micrograms/kg/day a rate of infusion known to produce hypertension. Five days of ACTH administration produced a progressive increase in plasma 17OHP from 0.45 +/- 0.12 to 128.9 +/- 28.4 nmol/l and in 17 alpha 20 alpha OHP from 0.54 +/- 0.15 to 73.1 +/- 7.2 nmol/l. Calculation of the blood production rate of both steroids during ACTH treatment confirms that the rates of infusion of 17OHP (3.0 mumol/h) and 17 alpha 20 alpha OHP (1.5 mumol/h) used to produce hypertension, when infused together with the other major ovine adrenocortical steroids, produced plasma concentrations in the range as found following administration at a rate to increase blood pressure.     

Effect of ouabain on adrenal potassium balance in sheep.

A previous study revealed that ouabain caused a marked decrease in aldosterone secretion, but the adrenal K status was not clear from those data. The present study investigated the magnitude and time course of change in adrenal K balance when ouabain was administered into the adrenal arterial supply of the in situ adrenal of conscious sheep. Ouabain at an adrenal arterial plasma concentration of approximately 2.4 X 10(-4) M produced a striking negative adrenal K balance within 10 min of beginning the infusion. The adrenal continued to lose K during the 30-min infusion and for 30 min thereafter. The mean total K loss was 42.3 +/- 7.9 muequiv/adrenal (n = 11). Thirty minutes after ending the ouabain infusion, the adrenal began taking up K but had not recovered its normal K complement by 60 min.     

The rapid adjustment of renal sodium excretion to changes in dietary sodium intake in sheep

The rapidity with which the kidney alters sodium excretion (ENa) in response to changes in dietary Na was studied in Merino sheep by analyzing hourly ENa for three control days, and then for three days after a change in Na intake. On a control diet of 117 mmol Na, sheep had a pre-feeding ENa of 3.5 mmol/hr., a striking post-feeding natriuresis that began 2 hours after feeding (less than 0.01), peaked at 4 hrs. and then declined to pre-feeding levels 7 hrs. after feeding. When in balance on a high Na diet the feeding of a low Na meal resulted in marked depression of ENa within 4 hours after feeding. On a low Na diet, a 100 mmol Na meal resulted in an increase in ENa within 4 hours but a 50 mmol Na meal did not. Thus, the sensitivity of post-feeding natriuresis is between 50 and 100 mmols Na. As post feeding natriuresis is a naturally occurring physiological event it should provide a useful paradigm for the investigation of mechanisms controlling Na balance.