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Endothelium-dependent responses to platelets and serotonin in spontaneously hypertensive rats.
Author(s) -
Thomas F. Lüscher,
Paul M. Vanhoutte
Publication year - 1986
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.8.6_pt_2.ii55
Subject(s) - endothelium , contraction (grammar) , medicine , endocrinology , platelet , adenosine , adenosine diphosphate , serotonin , chemistry , thrombin , endothelium derived relaxing factor , platelet aggregation , receptor
We studied endothelium-dependent responses to substances released from aggregating platelets in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Rings of thoracic aorta with and without endothelium were taken from adult rats and suspended for isometric tension recording in organ chambers containing modified Krebs-Ringer bicarbonate solution. Aggregating platelets caused statistically similar contractions in rings without endothelium in both strains. In rings with endothelium from SHR the contractions were significantly more pronounced than in rings with endothelium from WKY. In contracted rings with endothelium, serotonin caused a slight relaxation at lower concentrations but contraction at higher concentrations; only contractions were seen in rings without endothelium. The higher concentrations of the monoamine caused contractions, which in the SHR but not in the WKY were larger in the presence than in the absence of endothelium. In both strains adenosine diphosphate induced concentration-dependent relaxation in rings with endothelium but not in those without it; at high concentrations of adenosine diphosphate, the relaxation responses were significantly smaller in the SHR than in the WKY. Endothelium-dependent relaxation in response to thrombin did not differ in the two strains. The increased contraction in response to aggregating platelets and serotonin and the decreased relaxation in response to adenosine diphosphate in the SHR suggest that functional changes occur in the endothelium in this model of hypertension, possibly because of the release of one or more endothelium-derived contracting factors.

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