Effects of fentanyl, injected into the hypothalamic supraoptic and paraventricular nuclei, in a water-loaded and ethanol-anesthetized rat

ABSTRACT-The effects of injection of substance P (SP) into the hypothalamic supraoptic vasopres sinergic nucleus (SON) in water-loaded and ethanol-anesthetized rats were examined. Keywords:Substance P, Antidiuresis, Supraoptic nucleus, Vasopressin, Substance P antagonist Substance P (SP), a member of the tachykinin family of bioactive peptides, is suggested to be a neurotransmit ter or a neuromodulator in the central and peripheral nervous system (1 3). Immunohistochemical studies have shown that SP terminals are found not only in the spinal cord (4) and the substantia nigra (5), but also in the hypothalamus (6, 7). Therefore, the involvement of SP in physiological functions in the hypothalamus such as stimulation of arginine-vasopressin (AVP), growth hor mone and prolactin release has been suggested (8 10).The hypothalamic supraoptic nucleus (SON), as well as the paraventricular nucleus (PVN), contains cell bodies of vasopressinergic neurons that synthesize and release AVP. Stimulation of vasopressinergic neurons by neuro transmitters and neuromodulators induces a release of AVP, eventually causing antidiuresis through the renal AVP (V2) receptors (11,12). By injecting various drugs into the SON or PVN, we have previously shown that cholinergic (13,14), adrenergic (15, 16) and enkephaliner gic mechanisms (17, 18) may control the urine outflow through a stimulation of AVP release.The vasopressinergic cell bodies in the SON or PVN make synaptic contact with SP-containing nerve termi nals (6). It was demonstrated that intraventricular injec tion of SP induced a prolonged antidiuresis in water-load ed rat (19) and an increase in firing frequency of the SON (20). However, the effect of SP microinjected directly into the vasopressinergic nuclei on the AVP release remains un clear. In this study, we examined the effects of SP and its analog [D-Pro2, D-Trp'°9]SP on the outflow, osmotic pres sure and AVP level of urine by injection into the SON in water-loaded and ethanol-anesthetized rats. The influ ences of pretreatments with AVP-receptor, SP-receptor and muscarinic receptor antagonists on the SP-induced antidiuresis were also examined. The present data showed that SP causes antidiuresis through the release of AVP. MATERIALS AND METHODS Animals and drugsMale Wistar rats, weighing 280-330 g, were used.

Section: Discussionsupporting

confidence: 65%

mentioning

confidence: 99%

Blockade of Retinal NMDA Receptors by Sodium Nitroprusside Is Probably Due to Nitric Oxide Formation

Ujihara

Akaike

Tsutsumi

et al. 1993

“…The experimental procedures have been described in detail elsewhere (19). Male SHR (230-385 g, 11 to 19 week-old), WKY (255-400g, 10 to 20-week-old) and Wistar rats (280 420 g, 9 to 11-week-old) were starved for about 18 hr, but allowed free access to water.…”

Section: Methodsmentioning

confidence: 99%

“…The heart rate was measured by an electrocardiograph (FD-14; Fukuda, Tokyo). Respiratory rate and rectal temperature were measured by thermister probes (SR-1155, Nihon Kohden Kogyo Co., Ltd. and MGA 111-219, Nihon Kohden Kogyo Co., Ltd.) (19).…”

Section: Methodsmentioning

confidence: 99%

Effects of β1 and β2-Adrenoceptor Agonists Applied into the Hypothalamic Paraventricular Nuclei of Spontaneously Hypertensive Rats on Urine Production

Tsushima

Fujimoto

Matsuda

1994

ABSTRACT-We investigated effects of ~-adrenoceptor agonists ((3,-selective: T-1583 and dobutamine, 132-selective: fenoterol, non-selective: isoproterenol) on urine outflow rate, blood pressure, heart rate, respiratory rate and rectal temperature. The drugs were applied into the paraventricular nuclei (PVN) of spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Wistar rats. Fenoterol and isoproterenol markedly decreased the urine outflow rate, compared with T-1583 and dobutamine in the rats. There was no marked difference among the three strains in responsiveness to fenoterol and isoproterenol. The antidiuretic effects of fenoterol were inhibited by a p2-selective antagonist, butoxamine, more markedly than a ,-selec tive antagonist, atenolol, in SHR; and the inhibitory effects of these drugs were partial in WKY. In Wistar rats, the effect of fenoterol was inhibited by a non-selective a-antagonist, timolol, but not by atenolol or butoxamine. A vasopressin antagonist (i.v.) did not diminish the antidiuretic effect of fenoterol. Fenoterol reduced the blood pressure in SHR and WKY, but not in Wistar rats. It was suggested that there were predominantly (32-adrenoceptors mediating antidiuresis in SHR. In WKY and Wistar rats, however, the 13-adrenoceptor subtypes mediating antidiuresis have yet to be determined. The ability of j3-adrenoceptor agonists to decrease urine outflow rates in SHR was not altered as compared to that in the control rats.~-Adrenoceptor-mediated antidiuresis was not due to vasopressin release.

“…injection of dynorphin or bremazocine, K-agonists, produces the oppo site effects (16,17). Also, we have reported the antidiuret ic effect induced by microinjection of morphine or fen tanyl into the nuclei (18,19). However, the roles of o agonists in the regulation are not well known.…”

mentioning

confidence: 99%

Effects of D-Ala2-D-Leu5-Enkephalin, Microinjected into the Supraoptic and Paraventricular Nuclei, on Urine Outflow Rate

Tsushima

Mori

Matsuda

1993

ABSTRACT-The effects of D-Ala2-D-Leu5-enkephalin (DADL, a o-opioid agonist), microinjected directly into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, on urine outflow rate, urinary osmotic pressure, blood pressure, heart rate, respiratory rate and rectal temperature were investigated in water-loaded and ethanol-anesthetized rats. The microinjection of DADL into both the nuclei decreased urine outflow rate in a dose-dependent manner with an increase in urinary osmotic pressure, but did not change the other recorded parameters. The DADL-induced antidiuretic effect in the SON was inhibited by naloxone, but not by atropine, phenoxybenzamine, timolol nor a vasopressin antagonist, d(CH2)5-D Tyr(Et)VAVP. The effect in the PVN was inhibited by naloxone, atropine, timolol and d(CH2)5-D Tyr(Et)VAVP, but not by phenoxybenzamine. These results suggest that DADL causes antidiuretic effects mediated through opioid receptors in both the SON and PVN, and the underlying mechanisms are different between them. Involvement of o-opioid receptors in the DADL-induced antidiureses was discussed.