α1-Adrenoceptor-induced contractility in rat aorta is mediated by the α1D subtype

Alpha‐1D adrenoceptors are involved in reserpine‐induced supersensitivity of rat tail artery

“…From these data, together with the high affinity of the alpha-1D AR subtype for catecholamines, it is possible that most of the alpha-1D AR subtype is sequestered or downregulated under sympathetically innervated conditions and that this process may be reversed by sympathetic denervation, resulting in an upregulation of the alpha-1D AR. It is also interesting to note in this regard, that the alpha-1D AR subtype can be readily detected in both functional and ligandbinding studies using the rat thoracic aorta (Buckner et al, 1996;Muramatsu et al, 1998;Tanaka et al, 2004). Importantly, this tissue is not sympathetically innervated (Table 1 in the present study; Berkowitz et al, 1971;Stassen et al, 1998).…”

“…These results strongly suggest that the supersensitivity produced by low concentrations of phenylephrine is produced via the alpha-1D AR, while such a supersensitive response is absent in the untreated artery segments (present study; Lachnit et al, 1997;Murata et al, 1999), indicating apparent switching of functionally dominant alpha-1 AR from alpha-1A to alpha-1D subtype by reserpine treatment. In this regard, it is interesting to note that the alpha-1D AR subtype is highly sensitive to catecholamines and phenylephrine as compared with the alpha-1A and alpha-1B AR subtypes (Lomasney et al, 1991;Buckner et al, 1996;Graham et al, 1996). Additionally, the pEC 50 value (7.170.1) for phenylephrine in the reserpine-treated tail artery was the same as the pEC 50 value (7.270.1) in the thoracic aorta, where the adrenergic responses to phenylephrine have been known to be mainly mediated through alpha-1D ARs, irrespective of reserpine treatment (present study; Buckner et al, 1996;Muramatsu et al, 1998;Murata et al, 1999;Daly et al, 2002).…”

“…In this regard, it is interesting to note that the alpha-1D AR subtype is highly sensitive to catecholamines and phenylephrine as compared with the alpha-1A and alpha-1B AR subtypes (Lomasney et al, 1991;Buckner et al, 1996;Graham et al, 1996). Additionally, the pEC 50 value (7.170.1) for phenylephrine in the reserpine-treated tail artery was the same as the pEC 50 value (7.270.1) in the thoracic aorta, where the adrenergic responses to phenylephrine have been known to be mainly mediated through alpha-1D ARs, irrespective of reserpine treatment (present study; Buckner et al, 1996;Muramatsu et al, 1998;Murata et al, 1999;Daly et al, 2002).…”

“…These subtypes distribute distinctly and play key roles in adrenergic functions in many tissues (McGrath & Wilson, 1988;Muramatsu et al, 1995;Graham et al, 1996;Daly et al, 2002). In rats, for example, the adrenergic contraction of the tail artery is predominantly mediated by the alpha-1A AR subtype (Lachnit et al, 1997;Murata et al, 1999;Gisbert et al, 2003), while the adrenergic contractions of the thoracic aorta and spleen are mainly through alpha-1D and alpha-1B AR subtypes, respectively (Burt et al, 1995;Muramatsu et al, 1995;Buckner et al, 1996;Saussy et al, 1996). Recent studies further developed various drugs specific for each subtype.…”

“…BMY 7378 and KMD-3213 are well characterized as highly selective antagonists for alpha-1D and alpha-1A AR subtypes, respectively (Goetz et al, 1995;Shibata et al, 1995;Saussy et al, 1996;Yamagishi et al, 1996;Murata et al, 1999). Furthermore, several agonists including phenylephrine show relatively high affinity for the alpha-1D subtype (Lomasney et al, 1991;Buckner et al, 1996;Graham et al, 1996;Piascik & Perez, 2001). Stassen et al (1998) evaluated the relationship between the presence of adrenergic nerves and the presence of alpha-1 ARs in the arterial trees of rat, and suggested that the presence of alpha-1 AR subtypes may be closely related to the sympathetic innervation.…”