SUMMARY A new photoelectric sensor capable of detecting tail pulses even in unheated rats was tested for accuracy in indirect measurements of blood pressure. This sensor proved more sensitive than a Doppler ultrasonic flowmeter because it allowed detection not only of tail pulsations without preheating but also of peak oscillations usable for estimating mean arterial pressure. After blood pressures in anesthetized rats were elevated with norepinephrine or lowered with sodium nitroprusside, systolic pressures determined with the photoelectric sensor were almost identical with those recorded concurrently from femoral catheters (r = 0.939). Cuff pressure at peak oscillations in the tail correlated better with femoral mean pressure than with femoral diastolic pressure. However, similar comparisons in awake rats with chronically implanted carotid catheters showed that, although correlation between tail-cuff and carotid systolic pressures remained significant (r = 0.962), the correlation between peak tail oscillations and either mean or diastolic pressure was not. When systolic pressures were measured indirectly once a week for 7 weeks in unheated awake rats, normotensive rats could be easily distinguished from streptozotocin-diabetic and DOCA-salt hypertensive rats. (Hypertension 4: 898-903, 1982)

Interactions between abnormal salt intake and central sympathetic function were studied by recording pressor and sympathetic effects of hypothalamic stimulation in Dahl salt-resistant (DR) and salt-sensitive (DS) rats. All DS rats, including those fed a low-salt diet since weaning, became hypertensive by 11 weeks of age. Increased salt intake aggravated hypertension in DS rats without affecting blood pressure in DR rats. Basal sympathetic tone determined during urethane anesthesia, from the frequency of splanchnic nerve potentials as well as the magnitude of hypotension induced by a-adrenergic blockade with phentolamine, was consistently lower in low-salt DR rats than in any others. Pressor responses to electrical stimulation of the ventromedial hypothala-mus, whether expressed as absolute or percent increases in mean pressure, were invariably enhanced in DS rats. On the other hand, attendant increases in sympathetic nerve firing were significantly higher in DS rats, but only when expressed as absolute changes and not when expressed as percent changes. Consequently, pressor and sympathetic responses became dissociated in magnitude such that low-salt DR rats which had the weakest pressor responses also had the highest percent increases in sympathetic nerve firing. Peripheral increases in cardiovascular reactivity were considered unlikely because pressor responses to drugs like norepinephrine, tyramine, and vasopressin, were unaltered. Although 5-week-old DS rats that had not been exposed to high-salt intake remained normotensive, basal sympathetic activity and pressor responsiveness to hypothalamic stimulation were already enhanced. Since sympathetic and hypothalamic enhancement occurred before any other changes could be detected it was considered possible that sympathetic hyperactivity of hypothalamic origin may be involved in initiating genetic hypertension. These results also suggest that induction of hypertension in DS rats might depend on genetic transmission of hypersensitivity not only to salt but also to stressful stimuli. (Hypertension 5: 460-467, 1983) KEY WORDS • blood pressure • heart rate • high-salt diet • genetic hypertension • salt-sensitive Dahl rats • sympathetic hyperactivity • ventromedial hypothalamus A FTER Dahl and his associates succeeded in breeding two rat strains with opposite genetic predispositions to salt-induced hyperten-sion, they used parabiotic rats to show that the hyper-tension was due to a renal pressor substance. 1 2 Other mechanisms were not ruled out, however, and it remains possible that sympathetic dysfunction may also be involved. In Dahl salt-sensitive (DS) rats maintained on high-salt intake, vasoconstrictor responsiveness to sympathetic nerve stimulation becomes selectively enhanced as does the fall in vascular resistance resulting after sympathetic denervation. 3 Moreover, peripheral sympathectomy induced by either 6-hy-droxydopamine 4 or guanethidine 5 prevents subsequent elevation of blood pressure and vascular resistance. Concomitant elevation in DS rats of renal ...

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Benzoylaceton (I) reagiert mit Orthoameisensäureester (II) zum Äthoxymethylen‐Derivat (III), das mit Benzamidin (IV) zu den isomeren Pyrimidinylketonen (V) und (VI) cyclisiert wird.