Not a stimulus for normal/resting ventilation?

Ans is 'b' i.e. J receptor Guyton writes- "A few sensory nerve endings have been described in the alveolar walls in juxtaposition to the pulmonary capillaries--hence the name "J receptors". They are stimulated especially when the pulmonary capillaries become engorged with blood or when pulmonary edema occurs in such conditions as congestive heart failure. Although the functional role of the J receptors is not clear, their excitation may give the person a feeling of dyspnea. "Ventilation is controlled by group of neurons located in medulla and pons (described in detail in q. no. 18 Nov 2009). This rhythmic neural control is regulated by alterations in arterial PO2, PCO2 and PT ions concentration. These chemical controls are supplemented by a number of non-chemical influences (like Stretch receptors)The ultimate goal of respiration is to maintain proper concentration of oxygen, carbon dioxide, and hydrogen ions in the tissues.Stretch receptors: The stretch receptors are located in the walls of the bronchi and bronchioles throughout the lungs. They transmit signals through the vagi into the dorsal respiratory group of neurons when the lungs become overstretched, when the lungs become overly inflated, the stretch receptors activate an appropriate feedback response that "switches off" the inspiratory ramp and thus stops further inspiration. This is called the Hering-Breuer inflation reflex.(Note that Ganong writes that J receptors are also stimulated by hyperinflation of the lung)