2001
DOI: 10.1161/hy09t1.095761
|View full text |Cite
|
Sign up to set email alerts
|

Role Of Calcitonin Gene-Related Peptide and Substance P in Dahl-Salt Hypertension

Abstract: Abstract-Calcitonin gene-related peptide (CGRP) and substance P are known to play a counterregulatory role in acquired models of salt-dependent hypertension. In contrast, neuronal production of these peptides is decreased in the spontaneously hypertensive rat, which may contribute to the elevated blood pressure. To determine the role played by CGRP and substance P in Dahl-salt hypertension, 4-to 6-week-old male salt-resistant (DR) and salt-sensitive (DS) rats were divided into 4 groups (nϭ5/group) and pair-fed… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

2
11
0

Year Published

2002
2002
2015
2015

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 20 publications
(13 citation statements)
references
References 19 publications
2
11
0
Order By: Relevance
“…In addition to TRPV1 impairment, CGRP levels in DRG are similarly decreased, and CGRP-positive sensory nerves innervating mesenteric resistance arteries are remarkably reduced in DS rats fed an HS diet. This is in an agreement with a previous report from Katki et al, 15 which indicates that CGRP expression is reduced in DRG in DS rats. Given that the same reduction in CGRP-positive sensory nerve fibers is not observed in deoxycorticosterone acetate-salt-hypertensive rats that have similarly high blood pressure, the finding suggests that elevation in blood pressure may not be the cause of sensory nerve impairment.…”
Section: Discussionsupporting
confidence: 94%
“…In addition to TRPV1 impairment, CGRP levels in DRG are similarly decreased, and CGRP-positive sensory nerves innervating mesenteric resistance arteries are remarkably reduced in DS rats fed an HS diet. This is in an agreement with a previous report from Katki et al, 15 which indicates that CGRP expression is reduced in DRG in DS rats. Given that the same reduction in CGRP-positive sensory nerve fibers is not observed in deoxycorticosterone acetate-salt-hypertensive rats that have similarly high blood pressure, the finding suggests that elevation in blood pressure may not be the cause of sensory nerve impairment.…”
Section: Discussionsupporting
confidence: 94%
“…We have since extended these results to the DOC-salt model of hypertension, in which the neuronal expression and release of SP is increased as a compensatory mechanism to the elevated BP, 15 and in the DAHL-salt model (a genetic and salt-independent model of hypertension), in which SP does not seem to play a compensatory vasodilator role. 11 In addition, these data are in keeping with reports from the literature, which indicate reduced plasma levels of SP observed in the SHR and human essential hypertension 10 and the elevation of BP in these models could be due, at least in part, to the insufficient synthesis and release of endogenous SP.…”
Section: Discussionsupporting
confidence: 85%
“…Span-II has been previously shown to block the hypotensive effects of exogenously administered SP in normal rats. 11 For the present studies, each animal was anesthetized as described above. The left carotid artery was cannulated for continuous monitoring of mean arterial pressure (MAP) using a pressure transducer coupled to a recorder (Gould Instruments).…”
Section: Sp Receptor Agonist/antagonist Administration and Mean Artermentioning
confidence: 99%
“…However, the mechanisms responsible for the activation of the ET system remain to be elucidated. There is accumulating evidence showing that a defect in the sensory nervous system exists in spontaneously hypertensive rats and Dahl-salt sensitive hypertensive rats (33,17). Given the fact that ET-1 and the activation of ET A receptors contribute to the development of hypertension and renal dysfunction in sensory nerve-degenerated rats fed a HS diet, it is conceivable that sensory nerve dysfunction may contribute to the activation of the ET system in these models of hypertension.…”
Section: Discussionmentioning
confidence: 99%