AIM: This study investigates the subtypes of the alpha1-adrenoceptor mediating the adrenergically-induced renal vasoconstrictor responses in streptozotocin-induced diabetic and non-diabetic 2-kidney one clip (2K1C) Goldblatt hypertensive rats. METHODS: The renal blood flow responses to renal nerve stimulation, noradrenaline, phenylephrine, and methoxamine were measured in the absence and presence of nitrendipine, 5-methylurapidil, chloroethylclonidine and BMY 7378. RESULTS: The renal vasoconstrictor responses were markedly attenuated by nitrendipine and 5- methylurapidil in the diabetic rats (all P< 0.05). In the non-diabetic rats, these responses were markedly attenuated by nitrendipine, 5-methylurapidil, and BMY 7378 (all P< 0.05). In both experimental groups, chloroethylclonidine markedly accentuated the renal vasoconstrictions caused by all the adrenergic stimuli (all P< 0.05). CONCLUSION: These observations indicate that alpha 1A-adrenoceptor subtypes play a major role in mediating adrenergically-induced renal vasoconstriction in the diabetic 2K1C Goldblatt hypertensive rats. In the non-diabetic 2K1C Goldblatt hypertensive rats, contributions of alpha 1A and alpha 1D-adrenoceptor subtypes were proposed. Apart from post-synaptic alpha 1-adrenoceptors, both in the diabetic and non-diabetic 2K1C Goldblatt hypertensive rats, the potential involvement of presynaptic alpha 1- adrenoceptors is also suggested.
AIM: This study investigates the subtypes of the alpha1-adrenoceptor mediating the adrenergically-induced renal vasoconstrictor responses in streptozotocin-induced diabetic and non-diabetic 2-kidney one clip (2K1C) Goldblatt hypertensiverats. METHODS: The renal blood flow responses to renal nerve stimulation, noradrenaline, phenylephrine, and methoxamine were measured in the absence and presence of nitrendipine, 5-methylurapidil, chloroethylclonidine and BMY 7378. RESULTS: The renal vasoconstrictor responses were markedly attenuated by nitrendipine and 5- methylurapidil in the diabeticrats (all P< 0.05). In the non-diabeticrats, these responses were markedly attenuated by nitrendipine, 5-methylurapidil, and BMY 7378 (all P< 0.05). In both experimental groups, chloroethylclonidine markedly accentuated the renal vasoconstrictions caused by all the adrenergic stimuli (all P< 0.05). CONCLUSION: These observations indicate that alpha 1A-adrenoceptor subtypes play a major role in mediating adrenergically-induced renal vasoconstriction in the diabetic 2K1C Goldblatt hypertensiverats. In the non-diabetic 2K1C Goldblatt hypertensiverats, contributions of alpha 1A and alpha 1D-adrenoceptor subtypes were proposed. Apart from post-synaptic alpha 1-adrenoceptors, both in the diabetic and non-diabetic 2K1C Goldblatt hypertensiverats, the potential involvement of presynaptic alpha 1- adrenoceptors is also suggested.
Authors: Mohammed H Abdulla; Munavvar A Sattar; Nor A Abdullah; Abdul Hye Khan; Kolla R L Anand Swarup; Hassaan A Rathore; Raisa N Kazi; Fathihah Basri; Edward J Johns Journal: Ups J Med Sci Date: 2010-11-04 Impact factor: 2.384
Authors: Sheryar Afzal; Munavvar Abdul Sattar; Edward James Johns; Olorunfemi A Eseyin; Ali Attiq Journal: PPAR Res Date: 2021-10-14 Impact factor: 4.964