Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY(3-36), the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY(3-36) in rats. Peripheral administration of PYY(3-36) induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY(3-36) stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY(3-36) could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY(3-36)-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY(3-36)-induced reductions in feeding. This study indicates that peripheral PYY(3-36) may transmit satiety signals to the brain in part via the vagal afferent pathway.

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Atrial natriuretic peptide (ANP) is a member of the natriuretic peptide family that exerts various biological effects via acting on the receptor-guanylyl cyclase system, increasing the content of intracellular cyclic guanosine monophosphate (cGMP). ANP was first identified as a diuretic/natriuretic and vasodilating hormone, but subsequent studies revealed that ANP has a very important function in the inhibition of the renin-angiotensin-aldosterone system (RAAS), endothelin synthesis, and sympathetic nerve activity. Evidence is also accumulating from recent work that ANP exerts its cardioprotective functions not only as a circulating hormone but also as a local autocrine and/or paracrine factor. ANP inhibits apoptosis and hypertrophy of cardiac myocytes, and inhibits proliferation and fibrosis of cardiac fibroblasts. Reperfusion of the ischaemic myocardium by percutaneous coronary intervention (PCI) reduces the infarct size and improves left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, the benefits of PCI in AMI are limited by reperfusion injury. Animal studies have shown that ANP inhibits ischaemia/reperfusion injury, and reduces infarct size. We and others have recently shown that the intravenous administration of ANP inhibits RAAS, sympathetic nerve activity and reperfusion injury, prevents LV remodelling, and improves LV function in patients with AMI. ANP has a variety of cardioprotective effects and is considered to be a very promising adjunct drug for the reperfusion therapy in patients with AMI.

We investigated the antihypertensive effect of sesamin, a lignan from sesame oil, using two-kidney, one-clip (2K,1C) renal hypertensive rats. After clipping the left renal artery, animals were assigned to either a normal diet group (control group) or a sesamin-containing (1% (w/w)) diet group (sesamin group). The sham-operated rats (sham group) were fed a normal diet and tap water. The systolic blood pressure of the control group increased progressively in comparison with the sham group. This 2K,1C-induced hypertension was markedly reduced by feeding the sesamin-containing diet. The systolic blood pressure after 4 weeks was 123.60 +/- 4.01 mmHg in the sham group, 187.43 +/- 5.69 mmHg in the control group and 145.57 +/- 6.78 mmHg in the sesamin group, respectively. There were significant increases in left ventricle plus septum weight-body weight ratio in the control group compared with the sham group. This rise was also significantly reduced in the sesamin group. When the thoracic aorta was histochemically evaluated, the wall thickness and wall-to-lumen ratio in the control group were significantly increased, compared with the sham group, indicating that vascular hypertrophy had occurred in the control group. The sesamin diet tended to ameliorate this vascular hypertrophy, although its effect was not statistically significant. These findings suggest that sesamin is useful as prophylactic treatment to combat the development of renal hypertension and cardiac hypertrophy.

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