Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

Frame, Madeline H.; Hedqvist, Per

doi:10.1111/j.1476-5381.1975.tb06928.x

Cited by 67 publications

(25 citation statements)

References 25 publications

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“…15 Prostaglandin Ej (PGE2) is known to inhibit the release of norepinephrine by a prejunctional mechanism. 16 The released prostaglandin, however, does not contribute to inhibition of the pressor response to PNS. 5 Neuropeptide Y has some similarities to endothelin and might provide a clue to the mode of action of endothelin.…”

Section: Figure 1 Plotting Of Dose-response Curves For Effect Of Endmentioning

confidence: 99%

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

et al. 1990

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The effect of endothelin, a novel vasoconstrictor peptide, on the adrenergic neuroeffector junction was investigated in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The vasoconstrictor responses to periarterial sympathetic nerve stimulation and exogenous norepinephrine were determined. Infusion of endothelin-1 increased the baseline perfusion pressure dose dependentiy to similar extents in the two strains. A subpressor dose of endothelin-1 (10"'° M) enhanced the pressor response to norepinephrine; its effect was greater in WKY rats than in SHR. Endothelin-1 (10" to 10" M) attenuated the pressor response to sympathetic nerve stimulation, and the degree of inhibition tended to be less in SHR than in WKY rats. Higher doses (3xlO~" and 10 ' M) of endothelin-1 enhanced the pressor response to nerve stimulation in both WKY rats and SHR. Endothelin-1 inhibited norepinephrine release from rat mesenteric arteries; the inhibition was significantly less in SHR than in WKY rats. These results suggest that endothelin enhances the responsiveness of tt-adrenergic receptors to catecholamines, whereas it inhibits presynaptic adrenergic neurotransmission. Thus, endothelin can interact with the neuroeffector junction in addition to having a vasoconstricting effect in peripheral vessels. The difference in the mode of modulation by endothelin at the vascular neuroeffector junction in SHR from that in WKY rats might explain the maintenance of hypertension. (Hypertension 1990;15:739-743) E ndothelin was isolated from conditioned medium of cultured porcine aortic endothelial cells. 1 Recently, three forms of endothelin, named ET-1, ET-2, and ET-3, were identified by screening a human genomic library. 2 The extremely potent vasoconstrictor action of endothelin and the wide distribution of its binding sites, 3 including arteries, brain, and kidneys, suggest that it might be important in control of blood pressure as well as in the pathogenesis of hypertension. Recently, we found that ET-1 also has a neuromodulatory action in normotensive rats. -5To evaluate the contribution of endothelin to the maintenance of hypertension in the present study, we investigated its direct pressor action, its effect on the pressor responses evoked by exogenous norepinephrine and by periarterial nerve stimulation, and its effects on the release of norepinephrine from sympathetic nerve endings in perfused mesenteric arteries of spontaneously hypertensive rats (SHR).From the Department of Geriatric Medicine, Osaka University Medical School, Fukushima-ku, Osaka, Japan.Address for correspondence: Prof. Toshio Ogihara, Department of Geriatric Medicine, Osaka University Medical School, Fukushima-ku, Osaka 553, Japan. Methods AnimalsSHR (12 weeks old) and age-matched WistarKyoto (WKY) rats (Charles River Japan, Atsugi, Japan) weighing 289±3 and 300±5 g, respectively, and maintained on standard rat chow were used in the study. The systolic blood pressure and pulse rate of the rats were measured by the tai...

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Section: Figure 1 Plotting Of Dose-response Curves For Effect Of Endmentioning

confidence: 99%

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

et al. 1990

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“…Moreover, the absolute fall in outer cortical blood flow after indomethacin was greater than that in the middle cortex. This has been noted earlier by Kirschenbaum et al (1974), and may in part be due to reduced inhibition of noradrenaline released from sympathetic nerves following suppression of prostaglandin synthesis in the cortex (Frame & Hedqvist, 1975). This finding may be regarded as indirect evidence that renal prostaglandins play a supporting role in the circulation to not only the deep cortex, but also the superficial regions.…”

Section: Discussionmentioning

confidence: 50%

The effect of prostaglandin synthesis inhibitors on renal blood flow distribution in conscious rabbits.

Beilin¹,

Bhattacharya²

1977

The Journal of Physiology

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SUMMARY1. We have studied the effects of two prostaglandin synthesis inhibitors on renal cortical blood flow distribution in conscious rabbits.2. Renal blood flow distribution was estimated by means of radioactive microspheres injected into chronically implanted left atrial cannulae. Cardiac output was measured by a thermodilution technique.3. Measurements were made in groups of animals treated with either indomethacin, meclofenamate or control injections of phosphate buffer.4. A method of microtome slicing of the renal cortex was developed to standardize measurements. Microtome sections were grouped into inner, middle and outer zones. After both indomethacin and meclofenamate there was a reduction in total renal blood flow with a redistribution of flow from inner to outer cortex.5. Estimated renal vascular resistance rose in all three cortical zones. 6. The data support the hypothesis that renal prostaglandin synthesis is necessary for maintaining flow to the deep cortex. It is suggested that renal prostaglandins may also influence flow in more superficial zones. 7. Estimated total systemic vascular resistance was increased both with meclofenamate and indomethacin, suggesting an inhibiting effect of prostaglandins on arteriolar tone throughout a major part of the systemic circulation.

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“…, 1970Hedqvist et aI. , , 1971Sam uelsson and Wennmalm, 1971;Frame and Hedqvist, 1975). Second, sympathetic nerve stimulation re leases a prostaglandin-like substance into the splenic and renal venous effluents (Ferreira and Vane, 1967;Dunham and Zimmerman, 1970).…”

Section: Discussionmentioning

confidence: 99%

Role of Prostaglandins in Modulating Sympathetic Vasoconstriction in the Cerebral Circulation in Anesthetized Rabbits

Busija

1985

J Cereb Blood Flow Metab

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Summary:The effects of the interaction between sym pathetic nerves and prostaglandins in the cerebral circu lation were examined, The hypothesis tested was that inhibition of prostaglandin synthesis by indomethacin would potentiate decreases in CBF caused by sympa thetic nerve stimulation, In anesthetized rabbits, fol lowing administration of either indomethacin (10 mg/kg) or vehicle, CBF was measured with 15 -f.Lm microspheres prior to stimulation and following 3-5 min of electrical stimulation (4, 8, 16 Hz) of both superior cervical ganglia, In the vehicle group, CBF was 33-42 mIlmin/100 g prior to stimulation, Bilateral sympathetic stimulation reduced blood flow to the cerebrum by 12 ± 6% (mean ± SEM ) (p < 0,05 ) at 4 Hz (n = 8), by 20 ± 4% (p < 0,05 ) at 8 Hz (n = 12), and 21 ± 6% (p < 0,05 ) at 16 Hz (n = 11), In the indomethacin group, CBF was 37-48 mIlmin/100Prostaglandins and related compounds are syn thesized by cerebral arteries and have vasoactive effects (Ellis et aI., 1979; Abdel-Halim et aI., 1980). However, their importance in the regulation of CBF during physiological conditions is unclear. Although prostaglandins have been reported to participate di rectly in the maintenance of resting CBF and in cerebral vasodilatation during hypercapnia in rats and baboons (Pickard and MacKenzie, 1973; Dahl gren et aI. , 1981), recent studies were unable to con firm their involvement in these responses in rabbits, cats, and dogs (Wei et aI., 1980; Busija, 1983a;Busija and Heistad, 1983; Jackson et aI. , 1983 lation. Cerebral arteries are supplied richly by sym pathetic nerves (Nelson and Rennels, 1970;Peerless and Yasargil, 1978), and prostaglandins released near nerve endings during activation of sympathetic nerves could modulate cerebral vasoconstriction. Prostaglandins are synthesized and released by or near nerve endings during activation of sympathetic nerves, and appear to attenuate vasoconstrictor re sponses in several organs. For example, the blockade of prostaglandin synthesis by cyclooxy genase inhibitors results in augmented vasocon strictor responses during sympathetic nerve stimu lation in kidney and spleen (Ferreira and Moncada, 1971;Malik and McGiff, 1975; Oliver et aI., 1981). Only one previous study has examined this rela tionship in the cerebral circulation, and the results are paradoxical. Beausang-Linder (1982) reports that indomethacin, rather than augmenting re sponses, blocked decreases in CBF during sympa thetic nerve stimulation in rabbits. Limitations of that study were that sympathetic nerves were stim-

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Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

Cited by 67 publications

References 25 publications

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

The effect of prostaglandin synthesis inhibitors on renal blood flow distribution in conscious rabbits.

Role of Prostaglandins in Modulating Sympathetic Vasoconstriction in the Cerebral Circulation in Anesthetized Rabbits

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