Afferent nerves

The expression of TRPVl in the bladder is, however, not restricted to afferent nerves urothelium, detrusor muscle and fibroblasts also express TRPVl in the human bladder [140]. The implication of these findings for intravesical vanilloid therapy is unclear [141], but the increase in TRPVl immunoreactivity in the urothelium in patients with neurogenic detrusor overactivity (that occurs in concert with increased TRPVl in bladder af-ferents) is a very intriguing finding [142]. In the male urogenital system, TRPVl is also present in testicles, prostate and scrotal skin [143], and it was postulated that TRPVl ligands may be beneficial in the treatment of benign prostatic hyperplasia [144]. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

The taste bud is a polarized structure with a narrow apical opening, termed the taste pore, and basolateral synapses with afferent nerve fibers. Solutes in the oral cavity make contact with the apical membranes of the TRCs via the taste pore. There is a significant amount of lateral connectedness between taste cells within a bud both electrical synapses between TRCs and chemical synapses between TRCs and Merkel-like basal cells have been demonstrated to occur [39]. Furthermore, there are symmetrical synapses between TRCs and Merkel-like basal cells [39]. In addition, these basal cells synapse with the afferent nerve fiber, suggesting that they may function in effect as interneurons [39]. The extensive lateral interconnections... 

Stimulation of free nerve endings known as nociceptors is the first step leading to the sensation of pain. These receptors are found in both somatic and visceral structures and are activated by mechanical, thermal, and chemical factors. Release of bradykinins, K1, prostaglandins, histamine, leukotrienes, serotonin, and substance P may sensitize and/or activate nociceptors. Receptor activation leads to action potentials that are transmitted along afferent nerve fibers to the spinal cord. 

Nerves are bnndles of nerve fibers, connective tissne, and blood vessels. Each fiber is part of a nenron. Afferent nerves are entirely comprised of sensory nenrons and efferent (motor) nerves are comprised of motor nenrons. 

The ANS has sympathetic and parasympathetic branches. Both are made up of centrifugal (efferent) and centripetal (afferent) nerves. In many organs innervated by both branches, respective activation of the sympathetic and parasympathetic input evokes opposing responses. 

In the periphery, Hi-receptors on sensory neurons in the epidermis and dermis mediate itch and pain, respectively. Autonomic afferent nerve endings may be similarly stimulated by histamine. As in the CNS, presynaptic Hj-receptors act in a feedback inhibitory capacity. 

Increased vascular permeability and oedema Pulmonary artery vasoconstriction Coronary artery vasoconstriction Activation vagal afferent nerves in airways Bronchospasm Gut contraction... 

Neuronal nicotinic receptors are present on sensory nerve endings—especially afferent nerves in coronary arteries and the carotid and aortic bodies as well as on the glomus cells of the latter. Activation of these receptors by nicotinic stimulants and of muscarinic receptors on glomus cells by muscarinic stimulants elicits complex medullary responses, including respiratory alterations and vagal discharge. 

Stimulation of 5-HT4 receptors on the presynaptic terminal of submucosal intrinsic primary afferent nerves enhances the release of their neurotransmitters, including calcitoningene-related peptide, which stimulate second-order enteric neurons to promote the peristaltic reflex (Figure 62-4). These enteric neurons stimulate proximal bowel contraction (via acetylcholine and substance P) and distal bowel relaxation (via nitric oxide and vasoactive intestinal peptide). 

There is really only one, whole, integrated nervous system. However, for the purposes of understanding the effects of drugs and poisons on the system, we will subdivide it anatomically and functionally. Afferent nerves... 

Fleetwood-Walker, S. M., Mitchell, R., Hope, P. J., El-Yassir, N., Molony, V. The roles of tachykinin and opioid receptor types in nociceptive and non-nociceptive processing in superficial dorsal horn. In Fine afferent nerve fibers and pain, 1987, edited by R. F. Schmidt, H. G. Schaible, C. Vahle-Hinz, 239-247, VCH, Weinheim. 

Maggi, C. A. Tachykinins as peripheral modulators of primary afferent nerves and visceral sensitivity, Pharmacol. Res. 1997, 36, 153-169. 

The mechanism is not fully established, but possible mechanisms include delay in gastric emptying, activation of afferent nerves, and or central effects of GLP-1 receptor activation (9). It is dose related in the therapeutic range of doses and is more likely to occur in the first eight weeks (10,ll).Increasing the dose of exenatide gradually may be helpful (12). 

Nociception Prostaglandins Ej and E2 bring about the sensation of pain by sensitizing the afferent nerve endings to noxious chemical and physical stimuli. 

---