Almost all the physiological actions of angiotensin II, the effective mediator after renal renin has cleaved the precursor angiotensinogen and the angiotensin-converting enzyme (ACE) of the lung has liberated angiotensin II from angiotensin I, are mediated by by the angiotensin II type 1 receptor. It is a G-protein coupled receptor (GPcR) like many hormone receptors of the rhodopsin family (Omin 106165). Like many GPcR it has been difficult to crystallize to dertermine its threedimensional structure.
The depicted image is nothing compared to the images in the paper. You can, however, see how the ligand fits in a binding pocket in the transmembrane domain with its numerous helices. The domain on top is a extracellular domain.
The structure should help to resolve questions concerning the regulation of blood pressure, how mutations influence the binding of angiotensin II and may help to develop other drugs.
This is a very nice piece of work. Highly recommended!
Oxytoxin is the hormone of social interactions, the mechanism of the interaction mostly unknown. Therefore, it is a nice surprise that Nakajima, Görlich, and Heintz from the Rockefeller Univ. in New York report in Cell on a newly identified subset of somatostatin interneurons from the prefrontal cortex of mice which bear the oxytocin receptor.
They silenced then this receptor in some mice. The females in these silenced mice with the oxytocin receptor inactive lacked the social interactions with male mice only during the estrus phase, when copulation would ensure progeny. The interactions with female mice were normal. In the diestrus phase interactions with males were not disturbed.
Similarily they could produce mice where the oxytocin gene was removed in the prefrontal cortex. The female mice showed the same deficit. Even mice treated with an oxytocin antagonist blocking the action of oxytocin had the same effect on the social interactions of the females thus treated.
We do not know whether oxytoxin is acting here in an endocrine way via the blood or as a neurotransmitter via synapses. It is not to far fetched to think oxytocin stimulating these interneurons is required – in mice – for social interactions leading to progeny although it is not in the paper.
In the Journal of Molecular Endocrinolgy (Vol 52. No 3) there are several reviews on the evolution of G-protein coupled receptors: Secretin, CRH, Kisspeptin, Ghrelin, melanocortin, somatostatin/urotesin, and the 26 RFamide (GPR103). These reviews are obviously freely available.
I read them only cursory, however, I found very interesting relations of CRH from vertebrates, and diuretic hormones of insects which are going into the English version of the textbook on endocrinology.