ABSTRACT-We examined the effects of IV°-nitro-L-arginine (L-NNA) on isolated rabbit afferent arterioles to confirm that nitric oxide is released at the resistance vessel level in the kidney. We microdissected the superficial afferent arterioles from the kidneys of New Zealand White rabbits. Each afferent arteriole was cannulated with a micropipette system, and the intraluminal pressure was set at 80 mmHg. By our methods, we found that norepinephrine (NE) decreased the lumen diameter of the afferent arterioles in a dose-depend ent manner, and acetylcholine increased the lumen diameter of NE-constricted afferent arterioles. L-NNA (10-4 M) gradually decreased the lumen diameter of afferent arterioles from 21.5±0.9 to 18.6±0.9 pm in 20 min, but 1V°-nitro-D-arginine (10-4 M) did not affect them (from 21.8 ± 1.3 to 21.8 ± 1.5 pm). L-Arginine (10-2 M) restored the lumen diameter of L-NNA-contracted afferent arterioles to the control levels. These findings indicate that the isolated afferent arteriole has the ability to release or to synthesize and release nitric oxide under basal conditions and that this basal release of nitric oxide plays an important role in the basal tone of the afferent arteriole.
Abstract-Our purpose was to localize the intrarenal vascular sites of action of adenosine and glucagon. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured in anesthetized dogs, and renal perfusion pressure (RPP) was varied by an adjustable aortic clamp. At normal RPP, RBF was increased by all agents. In contrast, GFR was increased by glucagon, decreased by adenosine and unchanged by acetylcholine (ACh) or adenosine plus glucagon. The increases in RBF by glucagon occurred only at RPPs within the autoregulatory pressure range, and renal autoregulatory capability was attenuated during the infusion of glucagon. In contrast, adenosine increased RBF at RPPs both within and below the autoregulatory pressure range, and the autoregulatory capability was not perceptibly impaired. Superimposition of glucagon to adenosine caused further vasodilation, and the autoregulatory efficiency was completely attenuated. There was no difference between the RPP-RBF or RPP-GFR relations obtained during infusion of adenosine plus glucagon and ACh, which dilates both the afferent and efferent arterioles. It is generally accepted that afferent arteriolar resistance attains a minimum value at RPP near the lower limit of the autoregulatory range. Thus, our data indicate that glucagon and adenosine preferentially dilate the afferent arteriole and the efferent arteriole, respectively.
ABSTRACT-Paeoniflorin, a major constituent of peony root, has been demonstrated to attenuate the radial maze performance deficit produced by scopolamine. In the present study, to investigate the possible involvement of ~-adrenergic systems in the paeoniflorin antagonism of the scopolamine deficit, the effects of two ~-adrenoceptor antagonists, propranolol and atenolol, on the paeoniflorin effect were examined in male Wistar rats. Paeoniflorin (1 mg/kg, p.o.) significantly attenuated the scopolamine HBr (0.3 mg/kg, i.p.) induced deficit in the choice accuracy in radial maze performance without changing the running time pro longed by scopolamine. Neither D,L-propranolol HCl, a lipophilic p-antagonist, at 3 mg/kg, i.p. nor atenolol, a hydrophilic p1-antagonist that is known to hardly ever cross the blood-brain barrier, at 1 mg/kg, i.p. impaired maze performance by itself or aggravated the scopolamine-induced deficit in radial maze per formance. Both antagonists, however, completely blocked the antagonizing effect of paeoniflorin on the scopolamine deficit. These data suggest that the 3-adrenergic systems, especially peripheral ~1-adrenergic systems, are involved in the antagonizing effect of paeoniflorin on the scopolamine deficit in radial maze per formance in rats.
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