The influence of sex hormones on the development of left ventricular hypertrophy was investigated in baroreceptor-denervated rats. A significant increase ( p < 0.01) in the left ventricular weight/body weight ratio was observed in male but not in female rats 15 days after operation, compared to age-and sex-matched sham-operated rats. This differential hypertrophy occurred despite the development of a significant elevation in arterial blood pressure in both sexes. Castration prior to sinoaortic denervation did not change the level of arterial hypertension but caused a significant reduction (p<0.01) in left ventricular weight in male rats and a significant increase (p<0.01) in female rats. The pretreatment of male and female sinoaortic denervated and castrated rats with testosterone resulted in ventricular hypertrophy similar to that observed in intact male sinoaortic denervated rats. Pretreatment with estradiol, however, suppressed the left ventricular hypertrophy hi intact male rats but did not change the normal ventricular mass observed in intact female sinoaortic denervated rats. These results indicate that the development of left ventricular hypertrophy in sinoaortic denervated rats is modulated by sex hormones, and that testosterone exerts a facilitatory and estradiol an inhibitory action. (Hypertension 11 [Suppl I]: I-93-I-97, 1988) KEY WORDS • baroreceptors • neurogenic hypertension • heart rate • arterial pressure

No abstract

Synthetic bradykinin (SBR 640) was assayed on the isolated hearts of the guinea pig, the rabbit, the cat, the dog, and the rat. With the exception of the rat's heart, all reacted strongly to bradykinin with an increase in coronary flow. The guinea pig's heart was by far the most sensitive, reacting to concentrations of bradykinin of the order of 10 -9 to 10 -10 and therefore being as sensitive as the rat's uterus and rat's duodenum, so far the preparations most sensitive to bradykinin. On the dynamics of a normally beating heart, the effects of bradykinin are slight or trivial. When the amplitude or rate is reduced, bradykinin tends to increase both. There was, however, no relationship between its effects on the frequency or amplitude and its strong vasodilating effect on the coronary vessels. Since there was no tachyphylaxis to even threshold doses of bradykinin, the conclusion is drawn that it affects directly the coronary bed through its typical vasodilating action. The possibility of bradykinin being a mediator in the coronary vasodilation produced by epinephrine has been discussed.

Homogenates of rat heart when fortified with diphosphopyridine nucleotide (NAD) and adenylic acid (AMP) oxidize glucose to COo and HoO. 1 ' 2 This process is associated with a rapid formation of high-energy phosphate bonds. 3 ' 4 In this preparation occur all of the reactions involved in glycolysis, the tricarboxylic acid cycle, and high-energy phosphate formation and breakdown. Although this system is of great complexity, results obtained with it are highly reproducible and it permits investigation of the roles of different cellular elements and co-enzymes in the metabolism of a substrate.In earlier study it was observed that a rapid rate of glucose oxidation by the heart homogenate system occurred at a low concentration of ATP and it was concluded that the concentration of ATP present in the myocardium in vivo is far in excess of that necessary for efficient glucose oxidation. 8 In the present investigation the roles of the adenine nucleotides in the regulation of glucose metabolism in the heart homogenate were studied in more detail. It was found that ATP, when present in a sufficiently high concentration, inhibited glucose utilization and that this inhibition was overcome by magnesium ions. Microsomes were observed to stimulate glucose utilization and to exert this effect at least partly by catalyzing the breakdown of ATP. These studies form the substance of this report. MethodsMale Wistar rats weighing approximately 200 grams were used. After decapitation, the hearts were rapidly removed and washed in a medium consisting of 0.02 M sodium phosphate (pH 7.2) and 0.123 M KC1. After blotting on filter paper, the hearts were weighed on a torsion balance and homogenized in a glass homogenizer with 1.25 ml of the* above medium per 100 mg of tissue. The homogenate was filtered through gauze and used as such or employed for separation of tissue fractions. Incubation was carried out at 37° in air in stoppered Erlenmeyer flasks in a Dubnoff shaker. Each flask contained 0.5 ml homogenate, 0.5 ml 0.15 M KC1, and 0.2 ml of a solution consisting of nicotinamide, NAD, and varying amounts of adenine nucleotides and MgCIo. The exact composition of the reaction mixture varied with the individual experiment. At the end of a period of incubation, 3 ml 0.4 N perchloric acid was added to terminate the reaction. Inorganic phosphate and phosphate hydrolyzed by 1 N HC1 at 100° 'was determined by the method of Fiske and SubbaRow/' Glucose was measured by the glucose oxidase method. 0 ATP was determined by a specific enzymatic method in which the utilization of ATP in the phosphorylation of 3-phosphoglycerate was coupled to the oxidation of NADH and the reduction of 2,3 diphosphoglycerate in the presence of the appropriate enzymes. 7 ADP was measured by letting it react with phosphoenol pyruvate and reducing the pyruvate formed with NADH. After addition of myokinase, AMP was also determined by this method. 7 NADH was measured in a Beckman spectrophotometer.In the preparation of tissue fractions the homogenate was first centrifuged at ...

No abstract