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Neurogenic influences

The purpose of this report is to discuss known humoral substances, to examine each in the light of its possible relation to hypertension, and to consider other evidence, both direct and indirect, for the existence of such substances and for their chemical structures. Inquiry into the neurogenic influences of this condition and methods for neutralizing them will be discussed by others (6, 1 ). It must be remembered, however, that humoral pressor mechanisms are probably usually initiated by neurogenic ones, and therefore comprise only one link—even though the most important one—in the chain of events which lead to chronic hypertension. [Pg.5]

Much like what was described in heart and lung, neuropeptides may release histamine from mast cells, which in turn may act on presynaptic H3-receptors (Matsubara et al., 1992). In this regard, endogenous histamine exerts a two faceted influence on neurogenic inflammation, since this substance may also cause vasodilatation and rise in vascular permeability through the Hi-receptor/NO-pathway (Levi et al., 1991 Lassen et al., 1995). [Pg.88]

Many clinical observations indicate that neurogenic factors in some way influence the development and maintenance of essential hypertension. It has long been recognized that stressful situations may induce marked increases in both systolic and diastolic pressures which persist for varying periods of time (21, 38), and that hypertensives tend to have a characteristic type of personality (2, 99. Such individuals usually exhibit important components of repressed antagonism and anxiety. They do not find emotional outlets in overt acts, but rather their emotions are expressed through an increased activity of the sympatho-adrenal system with a consequent increase in blood pressure. Relief of psychic tension frequently produces salutary effects in these patients. Individuals who show hyperactive sympathetic vasomotor reflexes (as measured by the cold pressor test) are much more prone than the average individual to develop hypertension in later life (57). [Pg.25]

In summarizing evidence for the participation of deranged sympatho-adrenal ( neurogenic ) factors in human hypertension, it must be concluded that such factors have been conclusively demonstrated only in cases of pheochromocytoma, central nervous system trauma, and increased intracranial pressure. There is presumptive evidence that neurogenic factors may be important during the early, labile phases of essential hypertension and that the effects of this early sympatho-adrenal activity may lead to a persistent hypertension on a renal basis later in life. However, the development of hypertension through this or any other mechanism occurs only in individuals predisposed by some completely unknown, but probably hereditary, influence. [Pg.30]

Puehler W, Stein C. Controlling pain by influencing neurogenic pathways. Rheum Dis Clin North Am. 2005 31 103-113, ix. [Pg.197]

Macaluso A, McCoy D, Ceriani G, Watanabe T, BUtz T, Catania A, Lipton JM (1994) Antiinflammatory influences of alpha-MSH molecules central neurogenic and peripheral actions. J Neurosci 14 2377-2382... [Pg.509]

The role of skin nerves in NIICRs has been studied using capsaicin (frfl s-8-methyl-N-vanillyl-6-nonen-amide), which is known to induce a release of bioactive peptides, such as substance P, from the axons of unmyelinated C-fibers of sensory nerves. Pretreatment of the skin with capsaicin inhibits erythema reactions in histamine prick tests (Bernstein et al. 1981), but does not inhibit either erythema or edema elicited by benzoic acid or methyl nicotinate (Larmi et al. 1989a). This suggests that NIICRs to these model substances are not a type of neurogenic inflammation of the skin. Topical anesthesia inhibits erythema reactions to histamine, benzoic acid and methyl nicotinate, but it is not known whether the inhibitory effect is due to the influence on the sensory nerves only or whether the anesthetic also affects other cell types or regulatory mechanisms of immediate-type skin inflammation (Larmi et al. 1989a). [Pg.222]

Denervation and dysinnervation abnormalities are usually neurogenous (but, atypically, sometimes can be myogenous see Chapter 1). Conceptually, denervation is a complete loss of neural influence on the muscle fiber (which initially can be reversible by... [Pg.45]

Not only the biochemical components affect stem cell differentiation, differences in the physical properties such as elasticity may also impact cell fate decisions. The mechanical stiffness of the hydrogels may influence cell viability, proliferation, and function as it was shown that soft, medium, and rigid substrates are neurogenic, myogenic, and osteogenic, respectively (Engler et al. 2006). A more in-depth survey of microencapsulation techniques and criteria for engineering the stem cell microenvironment can be found in recent reviews (Metallo et al. 2007 Schmidt et al. 2008 Burdick and Vunjak-Novakovic 2009). [Pg.603]


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See also in sourсe #XX -- [ Pg.159 ]




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