The effects of hyperosmotic mannitol on vascular smooth muscle contractile responses and on 45Ca movements were examined in different isolated canine arteries. Prior exposure to 50 mM mannitol decreased contractile responses elicited with dopamine (DA) in helical strips of canine terminal mesenteric arteries (Tm) and decreased the contractile response elicited with potassium (K+) in both isolated left anterior descending (LAD) and circumflex coronary arteries. Tension responses induced by norepinephrine or DA in the Tm and K+ and prostaglandin F2 alpha in LAD were relaxed by subsequent exposure to mannitol. Mannitol increased the uptake of 45Ca in Tm arteries. Exposure of the Tm and branches of the LAD to mannitol during the washout of 45Ca resulted in a decrease in the rate of loss of 45Ca; the presence of either K+, Mg2+, or ethylenediamine tetraacetic acid during the washout did not prevent the observed mannitol-induced decrease in 45Ca efflux. These effects of mannitol on 45Ca efflux without a concomitant major change in net 45Ca uptake could be attributed to an increase in bound Ca2+ at relevant membrane sites or stores. Thus, hypertonic mannitol may alter contractile responsiveness of selected canine arteries by impeding the release of bound and/or sequestered Ca2+ and, in this manner, decreasing the Ca2+ concentration at the contractile elements.

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Effects of nitroprusside and D 600 on norepinephrine- and KCl-stimulated Ca++ activation and contraction systems in canine renal vein as compared to canine renal artery.

The effects of nitroprusside (NP) and D 600 on norepinephrine (NE)- and KCl-induced maximal contractions and unstimulated 45Ca uptake and efflux were delineated in canine renal vein (CRV) and compared with results in renal artery. In CRV, but not in renal artery, NE-induced contractions are usually associated with rhythmic oscillations in developed tension. Corresponding KCl-induced contractions are not associated with rhythmic activity and are depressed by 57% in the presence of phentolamine (PA). The calcium channel blocker, D 600, rapidly and extensively relaxed NE-induced contractions (86%) in CRV, but slowly and moderately relaxed similar responses in artery (46%). PA-resistant, KCl-induced contractions were equally sensitive to the relaxant effects of D 600 in CRV (73%) or artery (72%), but the rate of relaxation was much more rapid in CRV. Prior exposure to D 600 inhibited KCl-induced contractions in both CRV and artery (99 versus 91%, respectively). Similar prior treatment reduced NE-induced contractions (60%) in CRV, and prevented the development of any NE-dependent rhythmic activity. In renal artery, NE-induced contractions were unaffected by prior D 600 exposure. NP relaxed KCl-induced contractions 32% in the presence of PA in CRV, but had little effect on KCl-induced responses in artery (6%). Prior exposure to NP inhibited KCl-induced contractions 60-67% in CRV, which is approximately twice the inhibition seen in artery (31%). Relaxation of NE-induced contractions with NP in CRV and renal artery are (43% and 38%, respectively) approximately equal. In renal artery, responses to NE are less sensitive (1.6-fold) to prior NP exposure than in CRV. Prior exposure to NP or to NP plus D 600 reduced NE-induced contractions in CRV 37% and 96%, respectively. NP and D 600 were without effect on unstimulated 45Ca uptake in CRV. In CRV, D 600 had no effect on 45Ca efflux into a O-Ca++ solution, whereas NP decreased the rate of 45Ca efflux in a maintained manner. Thus, NP and D 600 appear to interfere with differing components of Ca++ entry and Ca++ release in CRV. However, these components are less readily differentiated and more interdependent than similar, well-defined and characterized components in arterial smooth muscle, and appear to be convergent.

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PubMedDate not supplied

Cutaneous necrosis from chemotherapy in a patient with an arteriovenous fistula.

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