Renal sodium handling after noradrenergic stimulation of the lateral hypothalamic area in rats

The participation of specific of special nephron segments in the renal control of sodium handling after adrenergic stimulation was investigated by determining lithium clearance in groups of 5-12 male Wistar rats (230-300 g) microinjected with noradrenaline into the lateral hypothalamic area (LHA). Microinjection of noradrenaline (12.5 to 100.0 nmol/ul) into the LHA promoted a significant decrease in proximal sodium reabsorption (control, 86.5 ñ 1.3; 12.5,81.4 ñ 2.4; 50.0, 75.4 ñ 1.8 and 100.0,77.2 ñ 1.7%) and a dose-related increase in distal sodium reabsorption (control, 13.4 ñ 1.6; 12.5, 18.4 ñ 1.25.0,26.9 ñ 2.9; 50.0,24.1 ñ 2.7; 100.0,22.1 ñ 1.9%) with no significannt changes inm creatinine clearance. Fractional sodium reabsorption after different noradrenaline concentrations was significantly reduced in the proximal nephron sites up to the concentration of 25.0 nmol/ul. Beyond this concentration, a smaller but progressive increase in fraqctional sodium reabsorption was observed in the post-proximal segment. These findings suggest an effective participation of proximal and post-proximal nephrons in natriuresis after lateral hypothalamic noradrenergic stimulation

Renal water handling evaluated by lithium clearance following adrenergic and cholinergic stimulation of the lateral hypothalamic area

Male Wistar rats weighing 230-3--g were used to characterize the participation of adrenerg and cholinergic receptors of the lateral hypothalamic area (LHA) in the control of renal water excretion. Since stimulation of adrenergic or cholinergic receptors has no effect on glomerular filtration rate, the antidiuresis and significant delay in urinary flow observed after lateral hypothalamic stimulation with carbachol (CCh) (0.036 ñ 0.005 to o.019 ñ 0.003 µlmin-1 100g body weight-1) and noradrenaline (Nad) (0.024 ñ 0.005 to 0.025 ñ 0.004 µl min-1 100g body weight-1) are secondary to an increase in distal tubular fluid reabsorption (DFR). Data are reported as means ñ SEM for ten rats each group. Tubular water measured by lithim clearance demonstrated that LHA stimulation with CCh (2.8 nmol in 1 µl) and Nad (30.0 nmol in µl) leads to a significant reduction in proximal water reabsorption with CCh, 93.3 ñ 2.6 to 85.4 ñ 1.4%; Nad, 92.7 ñ0.9 to 88.6 ñ 1.3%), with a simultaneous and significant incrase in fluid reabsorption along the post-proximal nephrom segments when compared to control (CNa) (CCh, 6.7 ñ 0.7 to 14.5 ñ 1.1%; Nad 8.2 ñ 0.8 to 11.4 ñ 1.6%) These effects are blocked by muscarinic (atropine, 5 nmol in 1 µl) and alpha-1 adrenoceptors (prazosin, 4 nmol in 1 µl) antagonists. The results indicate the effective participation of the post-proximal nephron in the antidiuresis occurring after cholinergic and adrenergic LHA stimulation

Inhibition of gastric acid secretion by cholinergic stimulation of the lateral hypopthalamic area

Cholinergic stimulation of the lateral hypothalamic area with carbachol (1 microng in 1 micronl) markedly inhibited gastric acid secretion in the anesthetized rat. Inhibition was bloced by prior microinjection of atropine (4 microng/micronl) into the same brain area and was accompanied by an increased soldium content in the stomach. Muscarinic receptor mediated cholinergic inhibitory influence of the hypothalamus on gastric acid secretion is suggested by these results

Effects of injection of selective adrenergic receptor antagonists into the lateral hypothalamic area on renal function

Studies were underlaken to characterize the participation of specific alpha-1, alpha-2 and beta adrenoceptors of the lateral hypothalamic area *LHA) in the urinary excretion of sodium and potassium. Alpha-1 and alpha-2 IHA receptors were shown to participate in the regulation of renal sodium and potassium excretion. the effects of noradrenaline microinjection (30 nmol in 1 micronl) into the LHA on urinary sodium excretion (UNaV) are blocked by previous injection of the alpha-1 antagonist prazosin (4 nmol in 1 micronl) from 3.22 ñ 0.25 to 0.59 ñ 0.04 micronEq min-1 100g body weigh-1. Pre-injection of yohimbine, an alpha-2 antaghonist (4 nmol in 1 micronl), synergistically potentiated the action of noradrenaline on UNaV (3.22 ñ 0.25 to 4.02 ñ0.27 micronEq min-1 100g body weight-1) and on urinary potassium excretion (UKV) (0.70 ñ 0.08 to 1.15 ñ 0.12 micronEq min-1g body weight-1). The beta-adrenergic blockers metoprolol (100 nmol in 1 micronl) and propranolo (100 nmol in 1 micronl) had no sunergistic or antagonistic action on the sodium excretion fraction, suggesting that neither of these recptors in present in the LHA. Our results indicate that natriuresis occurs even in the absence of changes in glomerular filtration rate and demonstrate an inhibitory natriuretic effect of an alpha-1 blocker (prazosin) injected into the LHA before adrenaline, wile an alpha-2 antagonsit (yohimbine) yielded a potentiating effect (AU)ñ