Angiotensin Epinephrine

Many hormones and other blood-borne substances (including drugs) also alter contractile activity of smooth muscle. Some of the more important substances include epinephrine norepinephrine angiotensin II vasopressin oxytocin and histamine. Locally produced substances that may alter contraction in the tissue in which they are synthesized include nitric oxide prostaglandins leukotrienes carbon dioxide and hydrogen ion. 

Smooth muscle differs from skeletal muscle in various ways. Smooth muscles—which are found, for example, in blood vessel walls and in the walls of the intestines—do not contain any muscle fibers. In smooth-muscle cells, which are usually spindle-shaped, the contractile proteins are arranged in a less regular pattern than in striated muscle. Contraction in this type of muscle is usually not stimulated by nerve impulses, but occurs in a largely spontaneous way. Ca (in the form of Ca -calmodulin see p.386) also activates contraction in smooth muscle in this case, however, it does not affect troponin, but activates a protein kinase that phosphorylates the light chains in myosin and thereby increases myosin s ATPase activity. Hormones such as epinephrine and angiotensin II (see p. 330) are able to influence vascular tonicity in this way, for example. 

Angiotensin II also interacts with the autonomic nervous system. It stimulates autonomic ganglia, increases the release of epinephrine and norepinephrine from the adrenal medulla, and—what is most important—facilitates sympathetic transmission by an action at adrenergic nerve terminals. The latter effect involves both increased release and reduced reuptake of norepinephrine. Angiotensin II also has a less important direct positive inotropic action on the heart. 

Fig. 8. Known and potential interactions of the ACTH/adenylate cyclase/cyclic AMP-dependent protein kinase system in the adrenocortical cell with other hormones and intracellular messengers. Epinephrine activates adenylate cyclase in the adrenocortical cell [33]. Adrenocortical cells have receptors for several hormones which may activate G, including angiotensin II [34], acetylcholine [35], and endogenous opioid peptides [36]. Angiotensin II, acetylcholine and vasopressin [37-39] have all been demonstrated to activate the breakdown of PIP2 in adrenocortical cells and to stimulate steroidogenesis 5-hydroxytrypt-amine is also a known steroidogenic agent [40]. Probable receptor subtypes involved are indicated (/3 M (muscarinic) 5-HT, and V,). This is not a comprehensive diagramming of all stimuli or all possible interactions. Modified from Ref. 7.

Q2 The heart and blood vessels are innervated by sympathetic nerves. The fight or flight response of the sympathetic system is activated in stress, and epinephrine (adrenaline) is released into the blood. These responses increase the rate and force of the heart and constrict many blood vessels, both of which raise BP. In addition, continued sympathetic stimulation eventually causes structural changes in blood vessels, activation ofthe renin-angiotensin system and procoagulant effects. If stress is prolonged, these responses contribute to a sustained increase in BP. 

Non-channel synapses have membrane-bound neuroreceptors (which are not ion channels). When activated by the neurotransmitter they initiate an intracellular signalling pathway in particular they can alter the number and sensitivity of the ion-channel receptors in the same cell. These synapses are involved in slow and long-lasting responses such as learning and memory. Typical neurotransmitters are adrenaline (epinephrine), noradrenaline, dopamine, serotonin, endorphin, angiotensin and acetylcholine. 

Heart rate and systolic and diastolic blood pressures are greater in the upright than in the recumbent individual. The change in posture from lying to standing increases the secretion of catecholamines, aldosterone, angiotensin II, renin, and antidiuretic hormone. Epinephrine and norepinephrine concentrations in plasma may double within 10 minutes, but... 

Adenosine monophosphate, diphosphate, triphosphate Bradykinin Tachykinins Endothelin Unaffected Epinephrine Dopamine Isoproterenol Histamine Prostaglandin Az Prostacyclin Oxytocin Vasopressin Angiotensin II Activation Angiotensin I... 

Hori, K., Zhang, Q. H Saito, S Tanda, S Li, H. C and Suzuki, M. (1993) Microvascular mechanisms of change in tumor blood flow due to angiotensin-II, epinephrine, and methoxamine a functional morphometric study. Cancer Res. 53, 5528-5534. 

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