Angiotensin II and allostasis

Recently, we talked about allostasis, which is an extension of classical homeostatic regulation to include neural and hormonal signals that can reset homeostatic set points to anticipate changes in the environment.

As I was preparing to submit an abstract to Experimental Biology, which is the major conference in physiology, I realised that a paper that we published recently includes a potential example of allostatic regulation.

It turns out that the hormone angiotensin II that works to retain sodium and increase blood pressure also leads to increased production of the transcription factor NFAT5. This would be allostatic because when the kidney retains sodium the amount of sodium in the interstitial fluid in the medulla of the kidney increases, which means that its tonicity (the number of molecules per volume fluid) also increases and in turn causes osmotic stress. Normally, NFAT5 that is also known as Tonicity-responsive enhancer binding protein (TonEBP) reacts to changes in tonicity to activate genes that protect the cells. In this setting, it appears that the cells can anticipate increased tonicity by sensing angiotensin II directly and increasing the production of NFAT5 to be better prepared to respond to the change in osmotic stress that will come as an effect of the increased angiotensin II concentration.

I was happy to have the abstract well-received and actually got a talk, as well as a fair bit of interest at the poster.