Effects of hyperthermia on contraction and dilatation of rabbit femoral arteries

Abstract

To analyze the effect of hyperthermia on the vascular response, the isometric response of isolated rabbit femoral artery segments was recorded at 37 degreesC and hyperthermia (41 and 44 degreesC). Contraction to potassium (5 x 10(-3)-5 x 10(-2) M) was significantly greater at 41 and 44 than at 37 degreesC and increased by inhibition of nitric oxide (NO) synthesis with Nomega-nitro-L-arginine (L-NNA; 10(-4) M) or endothelium removal at 37 degreesC but not at 41 or 44 degreesC. Norepinephrine (10(-9)-10(-4) M) produced a concentration-dependent contraction greater at 41 or 44 than at 37 degreesC and not modified by endothelium removal or L-NNA at either temperature. Phenylephrine (10(-9)-10(-4) M) produced a contraction increased by warming to 44 degreesC but not to 41 degreesC. The specific alpha2-adrenoceptor agonist BHT-920 produced a weak contraction, reduced by the alpha1-adrenoceptor antagonist prazosin (10(-6) M) and increased at 44 degreesC but not at 41 degreesC. The concentration-dependent contraction to endothelin-1 (ET-1; 10(-11)-10(-7) M) was increased by warming to 41 and 44 degreesC and by endothelium removal or L-NNA at 37 degreesC but not at 41 or 44 degreesC. Response to ET-1 was reduced by endothelin ETA-receptor antagonist BQ-123 (10(-5) M) and ETB-receptor antagonist BQ-788 (10(-5) M). In arteries precontracted with ET-1 (10(-8)-3 x 10(-8) M), relaxation to sodium nitroprusside (10(-8)-10(-4) M) was increased at 41 and 44 degreesC vs. at 37 degreesC, but that of ACh (10(-8)-10(-4) M) or adenosine (10(-8)-10(-4) M) was not different at all temperatures studied. Relaxation to ACh, but not adenosine, was reduced similarly by L-NNA at all temperatures studied. These results suggest hyperthermia in muscular arteries may inhibit production of, and increase dilatation to, NO, resulting in unchanged relaxation to ACh and increased constriction to KCl and ET-1, and may increase constriction to stimulation of alpha1-adrenoceptors by NO-independent mechanisms.

Effects of cooling and warming on 5‐hydroxytryptamine‐ and acetylcholine‐induced contractions of human umbilical vessels: role of nitric oxide

“…The umbilical artery and vein vessels may belong to aberrant cutaneous vessels [31]. Furthermore, in different studies [7,8], it is reported that the effects of warming may be agent-specific; in our study, we observed the same results with 5-HT and ACh. On the other hand, there are conflicting reports about the contractile responses during cooling, because of the use of agents and tissues in noncutaneous vessels.…”

Hemodynamic responses to heat stress in the resting and exercising human leg: insight into the effect of temperature on skeletal muscle blood flow

“…The significant relationship implying a role of local hyperthermia upon limb microcirculatory control is consistent with reports from human forearm (5,6,19) and leg studies (24), showing that increases in local tissue temperature are tightly related to forearm and leg vasodilatation. However, the results from studies in isolated vessel preparations are equivocal with some reports showing an altered vascular responsiveness to elevations in temperature (23), while others do not (31). An alternative possibility is that local hyperthermia acted indirectly upon vasodilatation and sympatholysis through increases in intravascular ATP and/or other vascular signals sensitive to temperature.…”

Warming and response to contractile agents in calf cardiac vein: role of the nitric oxide

“…Massett et al [19] reported that, during warming the endothelium did not significantly alter the contractile responses to potassium chloride (KCl) and phenylephrine in rings from the mesenteric artery, however only KCl‐induced contractions were potentiated in endothelium‐denuded rings from the thoracic aorta. Moreover, it is reported that during warming, inhibition of nitric oxide synthesis did not modify the increased contraction to potassium, endothelin‐1 and norepinephrine, thus suggesting that the response to these vasoconstrictors is not modulated by nitric oxide during warming [18].…”