Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Abstract: The contractile action of cholecystokinin (CCK) on smooth muscle of the gut is either direct (gallbladder and gastric fundus) or both direct and neurally mediated (small intestine). These regional differences were used to characterize pharmacologically CCK receptors on smooth muscle cells and neurons of the gastric fundus, gallbladder, and ileum of the guinea pig. In circular and longitudinal ileal smooth muscle, tetrodotoxin was used to separate direct from neurally mediated contractile effects. Cholecystokinin receptors on smooth muscle cells were found in all locations. The muscle cells displayed a decreasing order of sensitivity to the C-terminal octapeptide of cholecystokinin as expressed in the median doses, and to the selective cholecystokinin antagonist, proglumide, as expressed in the inhibitory dissociation constants. The median doses of the octapeptide of cholecystokinin ranged from 5.5 nM in gallbladder muscle to 185 nM in circular ileal muscle; the corresponding inhibitory dissociation constants of proglumide ranged from 180 to 437 microM [corrected]. Cholecystokinin receptors on cholinergic neurons were confined to circular and longitudinal ileal muscle; the neurons were 80-300 times more sensitive to the octapeptide of cholecystokinin (D50's 0.5 and 2.3 nM) than the corresponding muscle cells, and 19-21 times more sensitive to proglumide (inhibitory dissociation constants, 20 microM [corrected]). The results provide clear evidence of cellular heterogeneity of cholecystokinin receptors (i.e., difference in sensitivity between muscle cells and neurons from the same location) as well as regional heterogeneity (i.e., difference in sensitivity between muscle cells from various locations).
Regional and cellular heterogeneity of cholecystokinin receptors mediating muscle contraction in the gut [published erratum appears in Gastroenterology 1987 Jun;92(6):2055]

Abstract: Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.
Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension.

Abstract: The purpose of this study was to define as a distinct clinical entity the syndrome of neurapraxia of the cervical spinal cord with transient quadriplegia. The sensory changes include burning pain, numbness, tingling, and loss of sensation, while the motor changes range from weakness to complete paralysis. The episodes are transient and complete recovery usually occurs in ten to fifteen minutes, although in some patients gradual resolution occurs over a period of thirty-six to forty-eight hours. Except for burning paresthesia, pain in the neck is not present at the time of injury and there is complete return of motor function and full, pain-free motion of the cervical spine. In our series, routine roentgenograms of the cervical spine were negative for fractures or dislocations in all patients. However, the roentgenographic findings did include developmental spinal stenosis in seventeen patients, congenital fusion in five patients, cervical instability in four patients, and intervertebral disc disease in six patients. Spinal stenosis was determined by two different roentgenographic methods. The first was the standard method, and the second was a ratio method devised by us. Both measurements were made at the level of the third through the sixth vertebral body on a routine lateral roentgenogram of the cervical spine that was available for twenty-four of the thirty-two patients and for a control group of forty-nine male subjects of similar age who did not have any neurological complaints. Using the ratio method, a measurement of less than 0.80 indicated significant spinal stenosis in the group of twenty-four patients for whom roentgenograms were available, as compared with a ratio of approximately 1.00 or more in the control group. There was statistically significant spinal stenosis (p less than 0.0001) in all of the patients as compared with the control subjects by both methods of determining spinal stenosis. A survey of 503 schools participating in National Collegiate Athletic Association (NCAA) football in the 1984 season found that 1.3 per 10,000 athletes had a history that was suggestive of neurapraxia of the cervical spinal cord. The phenomenon of neurapraxia of the cervical spinal cord occurs in individuals with developmental stenosis of the cervical spine, congenital fusion, cervical instability, or protrusion of an intervertebral disc in association with a decrease in the anteroposterior diameter of the spinal canal. We postulate that in athletes with diminution of the anteroposterior diameter of the spinal canal the spinal cord can, on forced hyperextension or hyperflexion, be compressed, causing transitory motor and sensory manifestations.(ABSTRACT TRUNCATED AT 400 WORDS)
Neurapraxia of the cervical spinal cord with transient quadriplegia.