Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study alterations of peripheral substance P (SP) and vasoactive intestinal peptide (VIP) in the immunoreactive nervous system in essential hypertension, plasma SP and VIP concentrations in stroke-prone spontaneously hypertensive rats (SHRSP) at 8, 12, 18, 28, 30, 35 and 48 weeks of age and age-matched Wistar-Kyoto rats (WKY) were measured, using enzyme immunoassays (EIAs). The mean plasma SP concentrations of SHRSP (n = 61) and WKY (n = 58) were 4.9 +/- 1.2 fmol/ml and 6.6 +/- 1.9 fmol/ml, respectively. The value of SHRSP was significantly lower than that of WKY (p < 0.01). The mean SP concentration of young SHRSP was significantly higher than those of other ages. The mean plasma VIP concentrations of SHRSP (n = 61) and WKY (n = 58) were 0.80 +/- 0.25 fmol/ml and 1.01 +/- 0.32 fmol/ml, respectively. The value of SHRSP was significantly lower than that of WKY (p < 0.01). These decreases in plasma SP and VIP concentrations of SHRSP were observed at all ages. Decreases in the peripheral release of SP and VIP from the endings of SP- and VIP-immunoreactive nerves of SHRSP were seen, and the functional involution of peripheral SP- and VIP-immunoreactive nerves in essential hypertension was suggested.
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PMID:Decreases in substance P and vasoactive intestinal peptide concentrations in plasma of stroke-prone spontaneously hypertensive rats. 751 29

The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) elicits vasodilation in the in situ peripheral microcirculation of hamsters with spontaneous hypertension and whether encapsulation of VIP into liposomes modulates this response. Using intravital microscopy, we found that suffusion of VIP (0.05 and 0.1 nmol) alone over cheek pouch resistance arterioles of normotensive hamsters elicited significant vasodilation that was potentiated and prolonged by encapsulation of the peptide into liposomes (P < 0.05). By contrast, VIP (0.5 and 0.1 nmol) had no significant effects on arteriolar diameter in hamsters with spontaneous hypertension. However, encapsulation of VIP into liposomes restored its vasorelaxant effects in hypertensive animals, although the duration of vasodilation was significantly shorter in comparison with controls (P < 0.05). Empty liposomes had no significant effects on arteriolar diameter in either group. These data indicate that VIP-induced vasodilation in the peripheral microcirculation in situ is impaired in essential hypertension and that encapsulation of VIP into liposomes restores, in part, this response.
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PMID:Encapsulation of VIP into liposomes restores vasorelaxation in hypertension in situ. 876 Jan 86