1. In order to determine if a sustained increase in cardiac output can lead to hypertension, seven conscious dogs were given a continuous infusion of dobutamine, a powerful stimulant of cardiac inotropism, into the left coronary artery for a 7 day period while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured.

2. The infusion technique (1·5 × 10−8 mol min−1 kg−1, intracoronary) was selected after short-term experiments showed that it increased cardiac output more effectively than intravenous infusion at the same rate.

3. The rise in cardiac output elicited by intracoronary infusion of dobutamine was largest during the first 6 h of the 7 days administration, at which time calculated peripheral resistance was decreased. Subsequently, cardiac output returned progressively toward its control value whereas mean arterial pressure remained elevated (by an average of 20–25 mmHg) and peripheral resistance increased significantly.

4. Measurements of blood and extracellular fluid volumes as well as plasma renin activity indicated that these factors were not involved in the blood pressure increase.

5. When the infusion was ended, arterial pressure fell rapidly but peripheral resistance remained elevated during the first 6 h. Cardiac output fell after 2 and 6 h to a value below that of the pre-infusion control. After 1 day and subsequently, blood pressure became normal, as did the peripheral resistance and cardiac output.

6. Both at the onset and offset transients of this model of hypertension, changes in cardiac output preceded changes in peripheral resistance. These experiments may give experimental support to the concept of cardiogenic hypertension.

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