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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The electrophysiological actions of several agonists which may differentiate between P2X1- and P2X3-receptors were studied under concentration and voltage-clamp conditions in dissociated neurones of 1-4 day old rat dorsal root ganglia. 2. Beta,gamma-Methylene-D-ATP (beta,gamma-me-D-ATP) (1-300 microM), diadenosine 5',5'''-P1,P5-pentaphosphate (AP5A) (100 nM - 300 microM), diadenosine 5',5'''-P1,P4-tetraphosphate (AP4A) (300 nM - 300 microM) and uridine 5'-triphosphate (UTP) (1 microM - 1 mM) all activated concentration-dependent inward currents with a latency to onset of a few ms. 3. The concentration-response curves for beta,gamma-me-D-ATP and AP5A and ATP had similar maximum values, while that for AP4A had a lower maximum. The concentration-response curve to UTP was shallow and did not reach a maximum. Beta,gamma-Methylene-L-ATP was virtually inactive. The rank order of agonist potency was ATP > AP5A approximately AP4A > beta,gamma-me-D-ATP > UTP > > beta,gamma-methylene-L-ATP. 4. The inward currents were inhibited by the P2-receptor antagonists suramin (100 microM) and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) (10 microM). PPADS also inhibited responses to ATP (800 nM) and alpha,beta-methylene ATP (2 microM) in a concentration-dependent manner. 5. This study shows that beta,gamma-me-D-ATP, AP5A, AP4A and UTP all act via a suramin- and PPADS-sensitive P2X-receptor to evoke rapid, transient inward currents in dissociated neurones of rat dorsal root ganglia. The very low activity of beta,gamma-methylene-L-ATP suggests that the agonists were acting at the P2X3-subtype to produce these effects.
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PMID:Pharmacological properties of P2X3-receptors present in neurones of the rat dorsal root ganglia. 963 Mar 57

In 1937, Drs. Moritz and Oldt described arteriolar injuries in the kidneys (and other viscera) in hypertension, across the age range, in both sexes, and, in different races. This hypothesis proposes that injuries to vasomotor nerves cause the arteriolar injury in the kidney in hypertension, (as well as that in the uterus in preeclampsia). Different patterns of perivascular hyalinisation in different viscera are clues to the varying causes and consequences of arteriolar injury. In the uterus there is a symmetrical, perivascular "halo of hyalinisation" that marks the lines of extension of regenerating, injured nerves to the placental bed, whereas in the kidney there is a disordered and asymmetrical "halo of hyalinisation" where persistent, and recurrent, increases in intravascular pressures interrupt development of regenerating nerves. Consequences of injuries to vasomotor nerves include releasing a "soup" of cytokines that cause regeneration of "new" nerves expressing primitive, pain and stretch receptors including TRPV-1 and P2X3 purinergic "stretch" receptors that may be significant in the afferent mechanism in preeclampsia. There is also concurrent, "background" hyperplasia of denervated tunica media and intima leading to narrowing of the arterioles and a further drive to hypertension through renal ischaemia (Goldblatt, 1942). These observations require support from animal studies and other investigations to establish causation. This hypothesis may provide a number of potential mechanisms that reinforce, or accelerate, the physiological processes that contribute to hypertension.
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PMID:The arteriolar injury in hypertension. 2940