Ischemia-induced peripheral arterial vasospasm role of α1- and α2-adrenoceptors

Paolo Sapienza, John D. Edwards, Andrea Mingoli, Patrick E. McGregor, Nicola Cavallari, Devendra K. Agrawal

Research output: Contribution to journalArticle

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Abstract

Ischemia produces functional and structural alterations in peripheral blood vessels. Our study was designed to investigate α-adrenoceptor modifications induced by prolonged ischemia and their role in enhancing the contractile response during reperfusion in canine femoral arteries. Unilateral vessel ischemia was created by double crossclamping a femoral artery and was maintained for 3 hr. Reperfusion was allowed for 1 hr. The contralateral femoral artery was utilized as a control. The vessels were harvested for contractile and binding studies. Isometric tension studies revealed that the magnitude of the maximum contractile response to norepinephrine (NE), potassium chloride (KCl), and methoxamine was 671 ± 82 mg/mm2 versus 245 ± 43 mg/mm2 (P <0.01), 485 ± 46 mg/mm2 versus 229 ± 62 mg/mm2 (P <0.05), and 486 ± 88 mg/mm2 versus 126 ± 38 mg/mm2 (P <0.01), respectively for ischemic and nonischemic femoral arteries. EC50 values showed that ischemic vessels were more sensitive to NE, KCl, and methoxamine (P <0.05). Sodium nitro-prusside induced concentration-dependent and complete relaxation in all arterial rings (100% relaxation) but the ischemic femoral artery showed less sensitivity (P <0.05). Binding studies showed that the number of binding sites (Bmax) for [3H]Prazosin and [3H]-Rauwolscine were significantly increased in ischemic versus nonischemic vessels (1261 ± 95 fmole/mg versus 704 ± 113 fmole/mg, P <0.03, and 490 ± 86 fmole/mg versus 175 ± 15 fmole/mg, P <0.04, respectively). Furthermore, a significant decrease in affinity (Kd) for [3H]Prazosin and [3H]Rauwolscine was observed in ischemic versus nonischemic tissues (9.4 ± 1.7 nM versus 4 ± 0.2 nM, P <0.02, and 6.4 ± 1.5 nM versus 1.8 ± 0.6 nM, P <0.01, respectively). The increase in canine femoral artery vasoreactivity, following prolonged ischemia, seems to be also due to an increased density and functional activity of α-adrenoceptors expressed by the ischemic arterial smooth muscle cells.

Original languageEnglish
Pages (from-to)192-196
Number of pages5
JournalJournal of Surgical Research
Volume62
Issue number2
DOIs
StatePublished - May 1996

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Femoral Artery
Adrenergic Receptors
Ischemia
Methoxamine
Yohimbine
Prazosin
Reperfusion
Canidae
Norepinephrine
Potassium Chloride
Smooth Muscle Myocytes
Blood Vessels
Sodium
Binding Sites

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Ischemia-induced peripheral arterial vasospasm role of α1- and α2-adrenoceptors. / Sapienza, Paolo; Edwards, John D.; Mingoli, Andrea; McGregor, Patrick E.; Cavallari, Nicola; Agrawal, Devendra K.

In: Journal of Surgical Research, Vol. 62, No. 2, 05.1996, p. 192-196.

Research output: Contribution to journalArticle

Sapienza, Paolo ; Edwards, John D. ; Mingoli, Andrea ; McGregor, Patrick E. ; Cavallari, Nicola ; Agrawal, Devendra K. / Ischemia-induced peripheral arterial vasospasm role of α1- and α2-adrenoceptors. In: Journal of Surgical Research. 1996 ; Vol. 62, No. 2. pp. 192-196.
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abstract = "Ischemia produces functional and structural alterations in peripheral blood vessels. Our study was designed to investigate α-adrenoceptor modifications induced by prolonged ischemia and their role in enhancing the contractile response during reperfusion in canine femoral arteries. Unilateral vessel ischemia was created by double crossclamping a femoral artery and was maintained for 3 hr. Reperfusion was allowed for 1 hr. The contralateral femoral artery was utilized as a control. The vessels were harvested for contractile and binding studies. Isometric tension studies revealed that the magnitude of the maximum contractile response to norepinephrine (NE), potassium chloride (KCl), and methoxamine was 671 ± 82 mg/mm2 versus 245 ± 43 mg/mm2 (P <0.01), 485 ± 46 mg/mm2 versus 229 ± 62 mg/mm2 (P <0.05), and 486 ± 88 mg/mm2 versus 126 ± 38 mg/mm2 (P <0.01), respectively for ischemic and nonischemic femoral arteries. EC50 values showed that ischemic vessels were more sensitive to NE, KCl, and methoxamine (P <0.05). Sodium nitro-prusside induced concentration-dependent and complete relaxation in all arterial rings (100{\%} relaxation) but the ischemic femoral artery showed less sensitivity (P <0.05). Binding studies showed that the number of binding sites (Bmax) for [3H]Prazosin and [3H]-Rauwolscine were significantly increased in ischemic versus nonischemic vessels (1261 ± 95 fmole/mg versus 704 ± 113 fmole/mg, P <0.03, and 490 ± 86 fmole/mg versus 175 ± 15 fmole/mg, P <0.04, respectively). Furthermore, a significant decrease in affinity (Kd) for [3H]Prazosin and [3H]Rauwolscine was observed in ischemic versus nonischemic tissues (9.4 ± 1.7 nM versus 4 ± 0.2 nM, P <0.02, and 6.4 ± 1.5 nM versus 1.8 ± 0.6 nM, P <0.01, respectively). The increase in canine femoral artery vasoreactivity, following prolonged ischemia, seems to be also due to an increased density and functional activity of α-adrenoceptors expressed by the ischemic arterial smooth muscle cells.",
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