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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Activation of the effector element (enzyme or a calcium channel) creates a second messenger and results in a cascade effect. Guanine nucleotide-binding proteins (G proteins), are embedded in the cell membrane and contain alpha, beta, and gamma subunits. These regulate the activity of enzymes or calcium channels important for second messenger production. Based on current knowledge, two primary second messenger systems can be activated: cAMP and Ca++/IP3 (Figure 3.1a, b). G-protein activation of the enzyme adenyl cyclase results in cAMP formation; in the Ca++/IP3 system, the G protein simultaneously activates inositol triphosphate (IP3) formation and opens Ca++ channels. The cAMP and Ca++/IP3 systems are complementary in some cells but can have opposite effects in other tissues (23, 108). For example, for liver glycogenolysis the effect is complementary, but contraction and relaxation of smooth muscle can require different second messengers. A third type of second messenger, cyclic guanosine monophosphate (cGMP), has been established in a few tissues (23, 108).
Immune Modulation In Sepsis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Janet M. J. Hammond, Peter D. Potgieter
Nitric Oxide Nitric oxide is a low-molecular-weight, membrane-permeable gas [90] that functions as a neurotransmitter [91], regulates vascular tone by activating soluble guanylate cyclase in vascular smooth muscle cells and causing an increase in the level of intracellular cyclic guanosine monophosphate [92], and inhibits platelet aggregation [93], and leukocyte adhesion [94]. In addition, at concentrations higher than those required for intercellular communication, NO has antitumor and antimicrobial activity [95]. Nitric oxide release is thought to be the final common pathway that leads to the hypotension and vascular dysregulation seen in septic shock.
Cholinergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar
Muscarinic agonists act on blood vessels and show generalized vasodilation due to availability of M3 receptors on the endothelial lining of the vessel. They show fall in BP though they do not have a parasympathetic supply. Stimulation of M3 receptors releases NO by the action of nitric oxide synthase on l-arginine. NO causes accumulation of cyclic guanosine monophosphate (cGMP) responsible for smooth muscle relaxation (Sneddon and Graham, 1992).
The efficacy and safety of tadalafil in the management of erectile dysfunction with diabetes and blood circulation issues
Published in The Aging Male, 2023
Jong Seung Lee, Seung-ho Hong, Hwa Yeon Sun, Hyunseung Jin, Byung Yeon Yu, Yong-jin Cho, Jin young Chang, Byung Wook Yoo
Normally, problems with erection can be treated with phosphodiesterase-5 (PDE-5) inhibitors (Viagra®_Sildenafil) which inhibit cyclic guanosine monophosphate (cGMP). Several studies exist on the relationship between diabetes and vascular disease. Hatzichristou et al. [9], in a placebo-controlled study, showed that daily therapy with a PED-5 inhibitor is effective in improving the satisfaction associated with sexual intercourse and overall treatment satisfaction in patients with diabetes. Nevertheless, this is the first study to examine its association with capillary blood circulation. By inhibiting PDE-5, cGMP levels are prolonged, and smooth muscle relaxation is improved. Sildenafil, tadalafil, and vardenafil are PDE-5 drugs used in clinical care. PDE5i improves the success of erectile intercourse in patients with diabetic ED [10]. To improve ED, the medication must be taken 1–2 h before sexual activity. dosage should be regulated because the high dosage can lead to side effects. The side effects of PDE-5 inhibitors include flushing, headache, indigestion, congested nose, and diarrhea. Furthermore, MI and heart attack can occur in men who take sildenafil for ED. However, a couple of studies have found these medications to be highly tolerable while being safe and effective for coronary artery disease [11].
Antioxidant-rich Terminalia catappa fruit exerts antihypertensive effect via modulation of angiotensin-1-converting enzyme activity and H2S/NO/cGMP signalling pathway in Wistar rats
Published in Biomarkers, 2023
Adeniyi A. Adebayo, Ayokunle O. Ademosun, Bukola C. Adedayo, Ganiyu Oboh
Regulation of endothelial vasculature through the soluble guanylate cyclase/cyclic guanosine monophosphate (sGC/cGMP) pathway is a critical approach for hypertension management (Kagota et al., 2006, Chalimoniuk et al., 2015). The cellular concentration of cGMP is controlled by an enzyme called phosphodiesterase-5 (PDE-5). Owing to the paramount role of cGMP in smooth muscle relaxation, inhibition of PDE-5 become necessary to maintain a steady concentration of cGMP in the endothelial cells, thus combating hypertension (Lim et al., 2015, Ezekian and Hill, 2019). The present study assessed the effect of dietary inclusion of Terminalia catappa fruits on PDE-5 activity in L-NAME-induced hypertension in Wistar rats. The PDE-5 activity was higher in hypertensive group compared with the control. However, treatment with Terminalia catappa fruits-supplemented diets exhibited inhibitory action against PDE-5, thereby could be effective in inducing smooth muscle relaxation. A mechanism that could be paramount to the observed effect on the hemodynamic parameters. Nevertheless, the potential role of secondary metabolites of Terminalia catappa fruits cannot be underestimated.
Signaling mechanisms of the platelet glycoprotein Ib-IX complex
Published in Platelets, 2022
Yaping Zhang, Samuel M Ehrlich, Cheng Zhu, Xiaoping Du
Both VWF and low-dose thrombin induce elevation of intracellular cGMP (cyclic guanosine monophosphate), which activates the cGMP-dependent protein kinase (PKG) [88]. cGMP plays biphasic role in platelet activation: low concentrations of cGMP generated in the early phase of platelet activation, via PKG, promote integrin activation and granule secretion mediated by GPIb-IX and other receptors [88,90]. High concentrations of cGMP and cGMP generated at later phases of thrombus formation inhibit platelet activation and limit the growth of platelet thrombi [88,91] via PKG and PKA-dependent signaling pathways [12]. The biphasic role of cGMP provides a potential explanation as to why GPIb-IX-mediated platelet activation is often seen as “measured” or “weak” and platelets adherent on the surface of a thrombus exposed to high shear appear less activated despite clear evidence of integrin activation.