Variant angina pectoris. Is the parasympathetic nervous system at fault?
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Glial cell line-derived neurotrophic factor (GDNF) and a related protein, neurturin (NTN), require a GPI-linked coreceptor, either GFR alpha1 or GFR alpha2, for signaling via the transmembrane Ret tyrosine kinase. We show that mice lacking functional GFR alpha2 coreceptor (Gfra2-/-) are viable and fertile but have dry eyes and grow poorly after weaning, presumably due to malnutrition. While the sympathetic innervation appeared normal, the parasympathetic cholinergic innervation was almost absent in the lacrimal and salivary glands and severely reduced in the small bowel. Neurite outgrowth and trophic effects of NTN at low concentrations were lacking in Gfra2-/- trigeminal neurons in vitro, whereas responses to GDNF were similar between the genotypes. Thus, GFR alpha2 is a physiological NTN receptor, essential for the development of specific postganglionic parasympathetic neurons.
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3 sheep of approximately 4 years of age were used in the experiments. In 2 sheep in the cervical part of trachea all the nervous branches reaching this organ were cut and the remaining sheep was control. The animals were alive for 21 days. The following material was sampled for investigations: medulla oblongata, cervical part of spinal cord, bilateral spinal ganglions from C1 to C8, bilateral nodus ganglion and zygomatic ganglion and left and right parts of the cervical vagus nerve. The material was fixed and cut into 15 micron sections and stained according to the modified method of Nissl. The experiments evoked vast regressive changes in the nervous cells of both central and peripheral nervous system which helped to determine the source of outlet of fibers innervating this organ. In this paper the sources of outlet for the parasympathetic nervous fibers were presented. It was found that parasympathetic nervous centers connected with trachea were located in 1/3 of the central part of nucleus parasympathicus, anterior to obex, so in this part of nucleus which is the main source of outlet for the esophageal dorsal trunk and the ventral vagus nerve.
The effects of atropine and beta-adrenoceptor blockers on mean HR, wave structure of the cardiac rhythm, and chronotropic reaction to noise stress were examined in cats. Atropine (0.5 mg/kg) increased the mean HR and significantly decreased the spectrum power of HF, LF, and VLF oscillations. The decrease in HF power was most pronounced, which enhanced LF/HF ratio. Propranolol (0.5 mg/kg) decreased the mean HR and slightly increased the power of HF, LF, and VLF oscillations. Atenolol (2 mg/kg) exerted similar but more pronounced effects. beta-Adrenoceptor blockers increased HF power to a greater extent than LF and VLF power, which led to a decrease in LF/HF ratio. Atropine markedly decreased the chronotropic reaction to stress. beta-Adrenoceptor blockers produced no effect on the amplitude of this reaction, but accelerated restoration of initial HR. It is established that the changes in power spectrum of HR and the phase reflex reactions in cats are mediated by parasympathetic influences; the sympathetic system is involved only in the control of mean HR, probably in response to the level of animal activity. The changes in LF/HF ratio during blockade of sympathetic and parasympathetic systems are caused by opposite influences of these systems on HF oscillations, but not by hypothetic "sympathetic" and "parasympathetic" nature of LF and HF oscillations of the heart rhythm.
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