Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 micrograms/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 micrograms/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction.
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PMID:Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina. 137 74

This study aimed to determine whether or not endothelium-dependent vasodilation is preserved in spastic segments of human epicardial coronary arteries. Segmental responses of coronary arteries to substance P were examined in 30 patients with variant angina and in 10 patients with atypical chest pain using a quantitative angiographic technique. Coronary diameter at the basal state was matched between spastic and non-spastic segments in patients with variant angina, normal coronary arteries and with atypical chest pain (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, 2.4 +/- 0.3 mm, respectively). In segments where vasospasm was induced by ergonovine and/or acetylcholine, changes in diameter in response to substance P did not differ from those in non-spastic segments; maximal dilation averaged 27.1 +/- 9.5% in the spastic segments and 24.4 +/- 9.6% in the non-spastic segments (expressed as a percent increase over the value before drug administration). It would appear that the potential of the endothelium to release endothelium-dependent relaxant factor (EDRF) and the vasodilator response to EDRF are preserved, even in spastic segments.
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PMID:Preserved endothelial function in the spastic segment of the human epicardial coronary artery in patients with variant angina--role of substance P in evaluating endothelial function. 750 36