Muscle peptide

R. F. Furchgott, in Vasodilatation Vascular Smooth Muscle, Peptides, Autonomic Nerves and Endothelium (Ed. P. M. Vanhoutte), pp. 401-414. Raven Press, New York, 1988. 

Furchgott, R. F. (1988). Studies on relaxation of rabbit aorta by sodium nitrite The basis for the proposal that the acid-activatable factor from bovine retractor penis is inorganic nitrite and the endothelium-derived relaxing factor is nitric oxide. In Vasodilatation Vascular Smooth Muscle, Peptides, Autonomic Nerves, and Endothelium (P. M. Vanhoutte, ed.), pp. 401-414. Raven, New York. 

Je, J. Y., Qian, Z. J., Lee, S. H., Byun, H. G., and Kim, S. K. (2008). Purification and antioxidant properties of bigeye tuna (Thunnus obesus) dark muscle peptide on free radical-mediated oxidation systems. J. Med. Food 11, 629-637. 

Day, T.A., Maule, A.G., Shaw, C. and Pax, R.A. (1997) Structure-activity relationships of FMRFamide-related peptides contracting Schistosoma mansoni muscle. Peptides 18, 917-921. 

Ignarro, L., Byms, RE, and Wood, KS. 1988. Biochemical and pharmacological properties of endothelium-derived relaxing factor and its similarity to nitric oxide radicals. Pages 427-436 In P. Vanhoutte, (ed.) Vasodilation Vascular smooth muscle, peptides, autonomic nerves, and endothelium. Raven Press, New York. 

The posterior lobe of the pituitary, ie, the neurohypophysis, is under direct nervous control (1), unlike most other endocrine organs. The hormones stored in this gland are formed in hypothalamic nerve cells but pass through nerve stalks into the posterior pituitary. As early as 1895 it was found that pituitrin [50-57-7] an extract of the posterior lobe, raises blood pressure when injected (2), and that Pitocin [50-56-6] (Parke-Davis) causes contractions of smooth muscle, especially in the utems (3). Isolation of the active materials involved in these extracts is the result of work from several laboratories. Several highly active posterior pituitary extracts have been discovered (4), and it has been deterrnined that their biological activities result from peptide hormones, ie, low molecular weight substances not covalendy linked to proteins (qv) (5). 

ANPs play an important role in the maintenance of cardiovascular homeostasis by counterbalancing the renin—angiotensin (RAS) system. ANP, the main circulating form of the natriuretic peptides, effectively relaxes vascular smooth muscle, promotes the excretion of sodium and water, and in the CNS inhibits vasopressin release and antagonizes AT-II induced thirst. 

Insulin is a peptide hormone, secreted by the pancreas, that regulates glucose metabolism in the body. Insufficient production of insulin or failure of insulin to stimulate target sites in liver, muscle, and adipose tissue leads to the serious metabolic disorder known as diabetes mellitus. Diabetes afflicts millions of people worldwide. Diabetic individuals typically exhibit high levels of glucose in the blood, but insulin injection therapy allows diabetic individuals to maintain normal levels of blood glucose. 

Mammals, fungi, and higher plants produce a family of proteolytic enzymes known as aspartic proteases. These enzymes are active at acidic (or sometimes neutral) pH, and each possesses two aspartic acid residues at the active site. Aspartic proteases carry out a variety of functions (Table 16.3), including digestion pepsin and ehymosin), lysosomal protein degradation eathepsin D and E), and regulation of blood pressure renin is an aspartic protease involved in the production of an otensin, a hormone that stimulates smooth muscle contraction and reduces excretion of salts and fluid). The aspartic proteases display a variety of substrate specificities, but normally they are most active in the cleavage of peptide bonds between two hydrophobic amino acid residues. The preferred substrates of pepsin, for example, contain aromatic residues on both sides of the peptide bond to be cleaved. 

Apelins and the Apelin Receptor. Figure 3 Scheme illustrating the hypothesised mechanisms of control of human (a) vasculartone and (b) cardiac contractility by apelin peptides ( ). In the vasculature, apelins (released via the small vesicles of the constitutive pathway) may act directly to activate apelin receptors on the underlying smooth muscle to produce vasoconstriction. This response may be modified by apelin peptides feeding back onto apelin receptors on endothelial cells to stimulate the release of dilators, such as nitric oxide. In heart, apelin peptides, released from endocardial endothelial cells, activate apelin receptors on cardiomyocytes to elicit positive inotropic actions. 

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