| Hypertension-associated hypalgesia (HAH) is presented for the first time in 1979, which attracted many scholars and clinical physicians. Different hypertensive animal models were used, such as spontaneously hypertensive rats (SHR), salt-sensitive (SS) hypertensive rats and experimentally hypertensive rats (EHR), including hypertensive rats by left renal artery clipping or induced by deoxycorticosterone acetate-salt administration or by receiving pressor agents, to study the threshold of nociceptive reflex. These results were basically in favor of the conclusion of HAH. However, recentlysome studies came to different outcomes. Though blood pressure was decreased to normal level after treatment by angiotensin-converting enzyme inhibitors and calcium antagonists, HAH couldn't be reversed. We found some phenomena that provided clues to solve these above questions from former relative references. (1) Lack of studies on long time course of observation on the changes of both blood pressure and threshold of nociceptive reflex. (2) Most of studies were on basic heat pain threshold. However, lack of studies on the threshold of mechanical nociceptive reflex which was more related to clinical pain. (3) Studies were done mainly on several spontaneously hypertensive animal strains. However, lack of comparative study on commonly experimentally hypertensive animals such as Sprague-Dawley(SD) rats.To study the effects of changes in arterial blood pressure on nociceptive reflex and pain sensitivity, we choose spontaneously (modeling clinically primary hypertension) hypertensive adult rats and experimentally (modeling clinically secondary hypertension) hypertensive adult SD rats by ligating left renal artery to discuss two following problems: (1) Under normal conditions, we observed the effects of changes in artery blood pressure on threshold of basic heat or mechanical nociceptive reflex in experimentally hypertensive animals. (2) Under normal conditions, whether the effects of long time course of continuous hypotention by reserpine on threshold of basic heat or mechanical nociceptive reflex were different or not.Experimentally (secondarily) hypertensive animal group: Adult male SD rats (n=17), weighing from 180-200g, were randomly divided into (1) sham group (n=4); (2) left-renal-artery-ligation group (n=8); (3) left-renal-artery- ligation + reserpine group (n=5). Under sodiumpentobarbital anesthesia (40mg/kg, i.p.), left renal artery was separated and ligated, and then sutured the incision. Blood pressure and the threshold of nociceptive reflex were parallelly measured from Day 1 after operation.Spontaneously (primarily) hypertensive animal group: 10 SHR were provided by Laboratory Animal Center of the Fourth Military Medicine University, but blood pressure of only 6 SHR reached the standard of diagnosing hypertension. Because SHR were genetically spontaneously hypertensive rats, we couldn't measure the threshold of nociceptive reflex before blood pressure increased and during the course of increase, and they were chosen in experiment 2.In the experiment, we used a radiant heat stimulator to stimulate bilateral hindpaws of rats, and recorded the time from stimulation to withdrawal reflex of rats, which was paw withdrawal thermal latency (PWTL, s); we used von-Frey fiber stimulator whose bending forces were ranked as 0.1, 0.4, 0.7, 2.5, 3.5, 4, 6, 8, 10, 12, 16, 25, 30, 40, 50, 60g to stimulate bilateral hindpaws of rats, and recorded a bending force being able to evoke 50% of the paw withdrawal occurrence expressed as paw withdrawal mechanical threshold (PWMT, g). Our results were as following:1. Effects of changes in arterial blood pressure on basic threshold of thermal and mechanical nociceptive reflex inEHRIn sham group, blood pressure temporarily increased on Day 1-3 after operation (141.0+6.55 mmHg vs. 120.8 +3.21 mmHg, n=4), but on Day 4, it came back to basic level (123.0+2.71 mmHg, n=4). However, inleft-renal-artery-ligation group, blood pressure started to rise from Da...
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