Key result
MEK inhibitor PD98059 restores perivascular adipose tissue-induced relaxation to ~45% in hypertensive rat aortas.
Why the study?
Perivascular adipose tissue regulates vascular tone via adipocyte-derived factors, and vascular MAPKs are implicated in hypertension, but whether MAPKs contribute to impaired adipocyte-derived factor-induced relaxation in hypertension remains unknown.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for MEK inhibition in hypertensive vascular dysfunction; leaves open human translation.
Background: Perivascular adipose tissue (PVAT) releases factors that regulate vascular tone (adipocyte-derived factors (ADFs) ). Mitogen-activated protein kinases (MAPKs) in blood vessels have been implicated in the development of hypertension. This study aimed to determine whether MAPKs are involved in impaired ADF-induced relaxation in hypertension.
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Arai‐Nakaya et al. (2022) studied Hypertension (n=12). PD98059 (MEK inhibitor) vs. Untreated SHR aortic rings was evaluated on Degree of relaxation of aortic rings without perivascular adipose tissue (-PVAT) by physiological salt solution from +PVAT rings (p=<0.001). Pretreatment of aortic rings from spontaneously hypertensive rats with the MEK inhibitor PD98059 restored perivascular adipose tissue-induced relaxation to levels similar to normotensive rats (45% vs -15%).
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