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M. E. Fitzgerald, C. Li, N. del Mar, A. J. Reiner; Stimulation of Hypothalamic Paraventricular Nucleus, Lateral Parabrachial Nucleus or Nucleus of the Solitary Tract Increases Choroidal Blood Flow in Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5018.
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The parasympathetic output of the superior salivatory nucleus (SSN) to the pterygopalatine ganglion (PPG) regulates choroidal blood flow (ChBF) via the nitrergic vasodilatory input of PPG to choroid. We have found that SSN is integrated into central cardiovascular circuitry, with SSN receiving inputs from such major vascular control cell groups as the paraventricular nucleus of the hypothalamus (PVN), the lateral parabrachial nucleus (PBL) and the nucleus of the solitary tract (NTS). The physiology of these cell groups suggests their input to SSN may help maintain ChBF during decreased systemic BP. The PVN is responsive to systemic blood pressure (BP) and helps maintain stable systemic BP. Similarly, the part of NTS that projects to SSN receives aortic baroreceptor input and responds to BP fluctuation, while PBL receives baroreceptive NTS input and mediates compensatory systemic vasoconstriction during low BP. We thus examined the influence of PVN, NTS and PBL on ChBF.
ChBF was measured transclerally from the superior aspect of the rat eye using laser Doppler flowmetry. Ipsilateral PVN, PBL or NTS were stimulated with 50-100 µA 0.5msec anodal pulse trains (100Hz) via a stereotaxically placed stainless steel stimulating electrode. Stimulation accuracy was subsequently confirmed histologically.
Stimulation of baroreceptive NTS yielded 150% ChBF increases, which were volume and velocity driven. Blood pressure decreased slightly during the NTS stimulation. PVN stimulation yielded a 100% ChBF increase that considerably outlasted the stimulation, and was volume and velocity driven. An increase in systemic BP accompanied the ChBF increase. Stimulation of PBL yielded volume and velocity driven ChBF increases of 100%. The increases were accompanied by a slight hypertensive BP effect, and were attenuated 75% by LNAME, suggesting the effect is mediated via a PBL input to SSN.
The present findings show that ChBF increases can be evoked by electrical activation of three neuron groups that project to SSN, namely PVN, NTS and PBL, each of which is involved in systemic vascular compensation for low BP. Our findings are consistent with the conclusion that these inputs are involved in helping maintain ChBF, via the parasympathetic output of SSN to PPG, during episodes of decreased systemic BP, such as occur normally during inactivity or sleep, or traumatically with blood loss.
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