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This study was designed to further discriminate alpha1-adrenoceptor subtypes in rat aorta and prostate using functional experiments. Responses induced by phenylephrine were equilibrated in both tissues. The pA2 values and slope factors of several alpha1-antagonists were assessed using concentration-response curves. The antagonists used were prazosin, WB-4101, 5-methylurapidil (5-MU), HV-723, and tamsulosin. In addition, the effects of chloroethylclonidine (CEC) and nifedipine on phenylephrine-induced contractions were investigated. A high pA2 value for prazosin was observed in both tissues (aorta 9.84, prostate 9.19) and the ranking of each drug's pA2 value is as follows: tamsulosin > prazosin > WB-4101 > HV-723 > 5-MU in the aorta, and tamsulosin > prazosin > 5-MU > WB-4101 = HV-723 in the prostate. A significant difference between the pA2 value of each drug except for tamsulosin in the aorta and in prostate was observed (p < 0.01). Inhibition of contraction by pretreatment with CEC was 83.9 +/- 2.42% in the aorta, and 6.17 +/- 0.94% in the prostate. On the other hand, inhibition of maximal response by pretreatment with nifedipine (1 micromol/l) was 35.1 +/- 2.2% in the aorta and 24.5 +/- 3.1% in the prostate. A good correlation between these pA2 values and pKi values for recombinant human alpha1b-adrenoceptor expressed in CHO cells (aorta) and alpha1a-subtypes of CEC pretreated rat hippocampus (prostate) were observed. In conclusion, these results suggest that: (1) the contraction of these two tissues is mediated by alpha1H-adrenoceptor with a high affinity for prazosin; (2) alpha1H-adrenoceptors correspond to alpha1b-(aorta) and alpha1a-subtypes (prostate), and (3) each alpha1-adrenoceptor subtype in the aorta and prostate may be alpha1b-(aorta) and alpha1a-subtypes (prostate), respectively.
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
January 1999,
European journal of pharmacology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
March 2006,
Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
June 1999,
European journal of pharmacology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
December 1995,
European journal of pharmacology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
September 2005,
General physiology and biophysics,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
February 2010,
Cellular and molecular life sciences : CMLS,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
November 1997,
British journal of pharmacology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
July 2005,
The Journal of urology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
June 1999,
European journal of pharmacology,
K Maruyama, and
M Suzuki, and
M Tsuchiya, and
Y Makara, and
K Hattori, and
T Ohnuki, and
K Watanabe, and
T Nagatomo
February 2002,
Biology of reproduction,
