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Endothelial dysfunction augments myogenic arteriolar constriction in hypertension
Hypertension (Dallas, Tex. : 1979)
|December 1, 1993
Summary
In hypertensive rats, arterioles constrict more in response to increased pressure. This heightened myogenic response is linked to enhanced production of endothelium-derived constrictor factors, particularly prostaglandin H2.
Area of Science:
- Vascular biology
- Hypertension research
- Physiology
Background:
- Increased peripheral resistance is a hallmark of hypertension.
- The myogenic response of arterioles plays a crucial role in regulating vascular tone and blood pressure.
Purpose of the Study:
- To investigate the pressure-diameter relationship (myogenic response) in arterioles from spontaneously hypertensive rats (SHR) compared to normotensive controls.
- To elucidate the role of endothelium-derived factors in the enhanced arteriolar constriction observed in early hypertension.
Main Methods:
- Isolated, cannulated cremaster muscle arterioles from Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and normal Wistar (NW) rats were studied.
- The pressure-diameter relation was assessed by stepwise increases in perfusion pressure.
- Experiments involved endothelium removal and the use of pharmacological inhibitors, including indomethacin, SQ 29,548, and CGS 13,080.
Main Results:
- Arterioles from SHR exhibited significantly enhanced constriction in response to increased perfusion pressure (60-160 mm Hg) compared to WKY and NW rats.
- Endothelium removal abolished this enhanced pressure-induced tone in SHR.
- SQ 29,548, a thromboxane A2-prostaglandin H2 receptor blocker, attenuated the enhanced myogenic response, while a thromboxane A2 synthesis inhibitor (CGS 13,080) did not.
Conclusions:
- Early hypertension is characterized by an increased pressure-induced arteriolar constriction.
- This phenomenon is primarily mediated by enhanced production of endothelium-derived constrictor factors, with prostaglandin H2 being a key contributor.