Complicated central effects of endothelin on blood pressure in rats.

Minamisawa, Kohsuke; Hashimoto, Ryuhei; Ishii, Masao; Kimura, Fukuko

doi:10.2170/jjphysiol.39.825

Cited by 11 publications

(4 citation statements)

References 18 publications

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“…Circulating endothelin was also found to influence the area postrema neurons. Minamisawa et al [1989], on the other hand, found a decrease followed by an increase of BP after ICV administration of ET in conscious rats. ET administered in the cisterna magna produced an immediate rise in the BP, renal nerve activity, and HR [Kuwaki et al, 1990a,b].…”

Section: Cardiovascular Systemmentioning

confidence: 89%

Endothelin mechanisms in the central nervous system: A target for drug development

Gulati

Srimal

1992

Drug Development Research

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Endothelin (ET), a vasoconstrictor peptide, was isolated and characterized in 1988. Since then extensive studies have been done in different animal species to identify its receptors in central nervous system (CNS) and peripheral tissues. Three forms of ETs have been identified: ET‐1, ET‐2, and ET‐3. Their distribution pattern and pharmacological functions have been defined. ET‐1 and ET‐2 are mainly distributed in the CNS, including spinal cord and the peripheral tissues, while ET‐3 although present in other tissues is mainly concentrated in the pituitary. ET receptors have been found to be coupled to intracellular pathways involving stimulation of Ca++ fluxes, through phospholipase C and inhibition of adenyl cyclase. The literature concerning central actions of ET has been reviewed. The bulk of the evidence shows that it may be a regulator of regional cerebral blood flow, and a modulator of the release of posterior pituitary hormones (oxytocin and vasopressin). It may also regulate the release of prolactin, growth, thyroid stimulating, or luteinizing hormones. The regulatory role of ET on cardiovascular system can be exerted by central as well as peripheral actions. Besides direct regulation, ET modulates the release of endothelium derived relaxing factor/nitric oxide (EDRF/NO) and increases the sensitivity of peripheral α‐adreno‐ceptors. Thus ET appears to establish a balance between vasodilatation induced by EDRF/NO release and vasoconstriction due to increased sensitivity of vascular a‐adrenoceptors. The level of ET was found to be raised in several pathological conditions like subarachnoid hemorrhage, myocardial infarction, cardiogenic and septic shock, Raynaud's disease, and pulmonary hypertension. Its level was also raised in patients undergoing chronic hemodialysis. On the other hand, the level of ET was significantly lower in the cerebrospinal fluid (CSF) of patients of depression. The available data suggest that ET has a neuromodulatory role in the CNS and may be involved in the pathophysiological processes of several diseases. ET mechanisms in the CNS could provide potential targets for the development of newer drugs. © 1992 Wiley‐Liss, Inc.

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Section: Cardiovascular Systemmentioning

confidence: 89%

Endothelin mechanisms in the central nervous system: A target for drug development

Gulati

Srimal

1992

Drug Development Research

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“…Increased activity of the sympathetic nervous system has long been recognized to play a role in SHR hypertension (8). Some reports have also suggested that AVP mediates the pressor response to ET-1 (17,18,21). However, ET-1 prompts equivalent increases in the Long Evans rat and its mutant counterpart, the Brattleboro rat, which lacks circulating AVP (27).…”

Section: E21mentioning

confidence: 99%

“…ET-1 injections into the lateral cerebral ventricle consistently increase systemic arterial pressure in rats, but the heart rate response varies (17,21,27,28,31). In contrast, intracisternal injection or application of ET-1 to the ventral medulla evokes a biphasic response, with an initial increase followed by a decrease in arterial pressure (6,14).…”

mentioning

confidence: 99%

“…Although blunted in the hypertensive state, the arterial baroreflex buffers the ET-1-induced pressor and AVP secretory responses in both strains. antidiuretic hormone; arterial baroreflex; blood pressure; spontaneously hypertensive rat; Wistar Kyoto rat INITIALLY IDENTIFIED AS POTENT vasoactive peptides (38), the endothelins (ET) are now recognized for their role in central regulation of cardiovascular function (4,5,17,21,22,31,32). Neuronal and nonneuronal ET mRNAs and peptides have been localized to hypothalamoneurohypophysial and medullary structures (14,20,33).…”

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confidence: 99%

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Endothelin-1 in hypertension in the baroreflex-intact SHR: a role independent from vasopressin release

Rossi

O’Leary

Woodbury

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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This study sought to identify whether central endothelin (ET) receptor activation contributes to the elevated pressure in spontaneously hypertensive rats (SHR) and whether an ET-stimulated vasopressin (AVP) release mediates the increased pressure. In Wistar Kyoto (WKY) rats, intracerebroventricular ET-1 induced a dose-dependent pressor response that was shifted rightward in SHR. ET(A) antagonism decreased mean arterial pressure in baroreflex-intact SHR (P<0.01), consistent with inhibition of endogenous ET-1, and blocked the pressor response to exogenous ET-1 in both strains. ET-1 increased AVP only after sinoaortic denervation (P<0.05). Contrary to WKY, sinoaortic denervation was required to elicit a significant pressor response with 5 pmol ET-1 in SHR. Sinoaortic denervation permitted ET-1 to increase AVP in both strains, and peripheral V(1) blockade decreased pressure in denervated but not intact rats. After nitroprusside normalized pressure in SHR, the pressor and AVP secretory responses paralleled those in WKY. Thus endogenous ET(A) receptor mechanisms contribute to hypertension, independent of AVP, in baroreflex-intact SHR. Although blunted in the hypertensive state, the arterial baroreflex buffers the ET-1-induced pressor and AVP secretory responses in both strains.

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NMDA receptor and NO mediate ET-1-induced behavioral and cardiovascular effects in periaqueductal gray matter of rats

et al. 2001

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Endothelin-1 (ET-1), a novel and potent vasoconstrictor in blood vessel, is known to have some functions in the rat central nervous system (CNS). In order to investigate the central functions of ET-1, ET-1 was administered to the periaqueductal gray area (PAG) of anesthetized rats to induce barrel rolling and increase the arterial blood pressure (ABP). ET-1 had a modulatory effect on central cardiovascular and behavioral control. The selective N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (3 micromol/kg, i.p.) blocked the ET-1 induced responses, and both the nitric oxide synthase (NOS) inhibitor L-NAME (N-nitro-L-arginine methylester 1 mmol/rat) and the nitric oxide (NO) scavenger hemoglobin (15 nmol/rat) had similar effects in reducing the ET-1 (10 pmol/rat)-induced behavioral changes and ABP elevation. However, NO donor sodium nitroprusside (SNP 10 microg, 1 microg/rat) decreased the ET-1 induced ABP elevation, and recovered the ET-1-induced barrel rolling effect that was reduced by MK-801. These results suggest that ET-1 might have neuromodulatory functions such as ABP elevation and barrel rolling induction in the PAG of the rats via the NMDA receptor and NO.

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Complicated central effects of endothelin on blood pressure in rats.

Cited by 11 publications

References 18 publications

Endothelin mechanisms in the central nervous system: A target for drug development

Endothelin mechanisms in the central nervous system: A target for drug development

Endothelin-1 in hypertension in the baroreflex-intact SHR: a role independent from vasopressin release

NMDA receptor and NO mediate ET-1-induced behavioral and cardiovascular effects in periaqueductal gray matter of rats

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